• Ballesteros_Tato_1Assistant Professor of Medicine

    Division of Clinical Immunology and Rheumatology

    Address:

    Shelby Building, Room 413
    1825 University Boulevard
    35294

    Telephone: (205) 975-4643

    Fax: (205) 975-3322

    Email: aballest@uab.edu

     

    Education:

    B.S. (Biology): Vigo University, Spain, 2001
    Ph.D. (Microbiology & Immunology): Universidad Autonoma de Madrid, Spain, 2007
    Postdoctoral Fellow:Trudeau Institute, Saranac Lake, NY, 2008
    Postdoctoral Fellow:University of Rochester, NY, 2008-2012.

     

    Research Interests

    The generation of long-lived, high affinity antibodies is required for protective immunity to most viruses and for protection after vaccination. Thus, it is essential to understand the mechanisms that control the generation of long-lasting protective antibody (Ab) responses. T follicular helper (Tfh) cells, a distinct CD4+ T cell subset that expresses high levels of CXCR5 and localizes in the B cell follicles, play an essential role on promoting long-lived Ab responses. In fact, in the absence of Tfh cells, long-term Ab responses are impaired and protection to pathogens compromised. Therefore, it is essential that we understand how to manipulate Tfh responses in order to improve the efficacy of vaccines. However, despite significant advances in the field, our understanding of how Tfh cells responses are initiated is very limited.

    Recent studies suggest that Tfh cells are initially primed by dendritic cells (DCs), suggesting that we may be able to develop adjuvants that preferentially activate DCs to promote Tfh cell priming or target vaccine antigens to those DCs that preferentially induce Tfh cells. Unfortunately, we do not know what signals direct the DCs to promote Tfh cell differentiation or which specific subsets of DCs prime Tfh cell responses. Thus, one of the goals of my lab is to determine the cellular interactions, the environmental cues and the molecular mechanisms that control the differential capacity of distinct populations of DCs to regulate Tfh cell responses in different models of infection and autoimmune disease. This knowledge will help us to determine the nature of adjuvants that can be used to boost Tfh cell responses to tumors, pathogens and vaccines.

    A second project in my lab focuses on the potential clinical benefits of low-dose IL-2 administration to treat autoimmune disease and the mechanisms underlying these effects. Recent studies indicate that low-dose IL-2 treatment suppresses unwanted immune responses in mice and humans, thus evidencing the potential of IL-2 to treat autoimmune disorders (reviewed by us in Immunotherapy. 2014). Increased regulatory T cell activity is one of the potential mechanisms by which low-dose IL-2 immunotherapy induces immunosuppression. However data obtained in my lab indicate that exogenous IL-2 administration prevents aberrant accumulation of Tfh and GC B cell in lupus-prone mice. Our results demonstrate an unexpected immunosuppressive function of IL- 2 that is independent on its role on Treg homeostasis, and provide an alternative mechanism to explain the clinical benefits of IL-2 immunotherapies to treat antibody-mediated autoimmune disorders. These data offer new insights into how polymorphisms in the IL-2 and IL-2R genes can affect self-reactive Tfh and B cell responses and influence the development of autoimmune disease manifestations. We are now exploring the potential therapeutic use of low doses of IL-2 in systemic lupus erythematosus, the potential synergistic effects of combining IL-2 administration with blockade of cytokine pathways that promote Tfh cell development and/or deplete B cells, and how more specifically target IL-2 to Tfh cells.

     

    Publications

    Click here for a complete list of publications. Below are a few selected papers.


    Ballesteros-Tato A
    , Randall TD, Lund FE, Spolski R, Leonard WJ, León B. 2016. T Follicular Helper Cell Plasticity Shapes Pathogenic T Helper 2 Cell-Mediated Immunity to Inhaled House Dust Mite. Immunity. 44(2):259-73. PMID: 26825674; PMCID: PMC4758890.


    Leon, B., Bradley, J.E., Lund, F.E., Randall, T.D. & Ballesteros-Tato, A. 2014. FoxP3+ regulatory T cells promote influenza-specific Tfh responses by controlling IL-2 availability. Nature communications 5, 3495 PMID: 24633065 PMCID: PMC4013682


    Ballesteros-Tato, A.
    , Leon, B., Lund, F.E. & Randall, T.D. CD4+ T helper cells use CD154-CD40 interactions to counteract T reg cell-mediated suppression of CD8+ T cell responses to influenza. 2013 The Journal of Experimental Medicine 210, 1591-1601. PMID: 23835849 PMCID: PMC3727323


    Ballesteros-Tato, A, 
     León, B, Graf, BA, Moquin, A, Adams, PS, Lund, FE, Randal, TD. 2012 Interleukin-2 Inhibits Germinal Center Formation by Limiting T Follicular Helper Cell Differentiation.  Immunity. 36: 847-856. PMID:22464171


    Ballesteros-Tato, A
    , B León, FE. Lund and TD. Randall. 2010. Temporal changes in dendritic cell subsets, cross-priming and costimulation via CD70 control CD8+T cells responses to influenza. Nat. Immunol. 11:216-224. PMID:20098442 PMCID:PMC2822886

  • BradleyProfessor of Medicine

    Address: 

    Shelby Building Room 177A
    1825 University Blulevard
    35294-2182

    Telephone:(205) 934-8550
    Fax:(205) 934-1564
    Email:braddog@uab.edu

     

    Education

    BA (Psychology), Vanderbilt University, 1971
    PhD (Clinical Psychology),Vanderbilt University, 1975
    Clinical Internship,Duke University Medical Center, 1975-1976

     

    Research Description

    Dr. Bradley's research focuses on the interactions among biological and psychosocial factors associated with abnormal pain sensitivity in persons with osteoarthritis (OA) of the knee, and other chronic painful disorders. Several studies are ongoing with support of an R01 grant and complementary grant funds: (1) In collaboration with investigators from the University of Florida, the goal of the R01 project is to characterize ethnic differences in experimental pain sensitivity, endogenous pain inhibition, clinical pain, and pain-related disability in older African-Americans and non-Hispanic whites with and without knee OA; (2) determine whether these measures of pain sensitivity/pain inhibition along with biological, psychological, and socio-cultural variables mediate ethnic group differences in clinical pain and pain-related disability; (3) examine the extent to which differences in pain responses between African-American and white patients with knee OA are mediated by group differences in biomarkers such as sleep disturbance or lipid mediators; and (4) examine the relationship between polysomnography measures of sleep and experimental as well as clinical pain to better understand the biological, psychological, and socio-cultural variables that mediate ethnic group differences in both sleep and pain.

     

    Publications

    Click here for a complete list of publications. Below are a few selected papers


    Bulls HW, Goodin BR, McNew M, Gossett EW, Bradley LA. 2016. Minority aging and endogenous pain facilitatory processes. Pain Med 17: 1037-1048. PMCID: PMC4896853


    Herbert MS, Goodin BR, Bulls HW, Sotolongo A, Petrov ME, Edberg JC, Bradley LA, Fillingim RB. 2016.  Ethnicity, cortisol, and experimental pain responses among persons with symptomatic knee osteoarthritis. Clin J Pain. 2016 Nov 28. [Epub ahead of print] PMID: 27898457


    Cardoso JS, Riley JL 3rd, Glover T, Sibille KT, Bartley EJ, Goodin BR, Bulls HW, Herbert M, Addison AS, Staud R, Redden DT, Bradley LA, Fillingim RB, Cruz-Almeida Y. 2016 Experimental pain phenotyping in community-dwelling individuals with knee osteoarthritis. Pain. 157: 2104-2114. PMCID: PMC4988907


    Neogi T, Guermazi A, Roemer F, Nevitt MC, Scholz J, Arendt-Nielsen L, Woolf C, Niu J, Bradley LA, Quinn E, Law LF. 2016. Association of joint inflammation with pain sensitization in knee osteoarthritis: The Multicenter Osteoarthritis Study. Arthritis Rheumatol. 68: 654-661. PMCID: PMC4827020


    Petrov ME, Goodin BR, Cruz-Almeida Y, King C, Glover TL, Bulls HW, Herbert M, Sibille KT, Bartley EJ, Fessler BJ, Sotolongo A, Staud R, Redden D, Fillingim RB, Bradley LA. 2015. Disrupted sleep is associated with altered pain processing by sex and ethnicity in knee osteoarthritis. J Pain.  pii: S1526-5900(15)00541-6. PMID: 25725172


    Glover TL, Goodin BR, King CD, Sibille KT, Herbert MS, Sotolongo AS, Cruz-Almeida Y, Bartley EJ, Bulls HW, Horgas AL, Redden DT, Riley JL 3rd, Staud R, Fessler BJ, Bradley LA, Fillingim RB. 2015. A cross-sectional examination of Vitamin D, obesity, and measures of pain and function in middle-aged and older adults with knee osteoarthritis. Clin J Pain. 12: 1060 - 1067  PMID: 25569220


    Neogi T, Frey-Law L, Scholz J, Niu J, Arendt-Nielsen L, Woolf C, Nevitt M, Bradley L, Felson DT, for the Multicenter Osteoarthritis (MOST) Study. 2015. Sensitivity and sensitisation in relation to pain severity in knee osteoarthritis: trait or state? Ann Rheum Dis 74: 682-688. PMID: 24351516 PMCID:PMC4062615


    Glass N, Segal NA, Sluka KA, Torner JC, Nevitt MC, Felson DT, Bradley LA, Neogi T, Lewis CE, Frey-Law LA. 2014. Examining sex differences in knee pain: the Multicenter Osteoarthritis Study. Osteoarthritis Cartilage. 22(8):1100-6. PMID: 24999111 PMCID: PMC4180745


    Petrov ME, Sawyer P, Kennedy R, Bradley LA, Allman RM. 2014. Benzodiazepine (BZD) use in community-dwelling older adults: Longitudinal associations with mobility, functioning, and pain. Arch Gerontol Geriatr. 59(2):331-7. PMID: 24880195 PMCID: PMC4130769


    Cruz-Almeida Y, Sibille KT, Goodin BR, Petrov ME, Bartley EJ, Riley JL, King CD, Glover TL, Sotolongo A, Herbert MS, Schmidt J, Fessler BJ, Staud R, Redden D, Bradley LA, Fillingim RB. 2014. Racial and ethnic differences in older adults with knee osteoarthritis. Arthritis Rheum 66:1800-1810 PMID: 24729357 PMCID: PMC4077911


    Goodin BR, Bulls HW, Herbert MS, Schmidt J, King CD, Glover TL, Sotolongo A, Sibille KT, Cruz-Almeida Y, Staud R, Fessler BJ, Redden DT, Bradley LA, Fillingim RB. 2014. Temporal summation of pain as a prospective predictor of clinical pain severity in adults aged 45 years and older with knee osteoarthritis: ethnic differences. Psychosom Med. 76(4):302-10. PMID: 24804882 PMCID: PMC4066647


    Riley III JL, Cruz-Almeida Y, Glover TL, King CD, Goodin BR, Sibille KT, Bartley EJ, Herbert MS, Sotolongo A, Fessler BJ, Redden DT, Staud R, Bradley LA, Fillingim RB. 2014. Age and race effects on pain sensitivity and modulation among middle-aged and older adults. J Pain 15: 272–282 PMCID: PMC4005289


    Ruiter Petrov ME, Lichstein KL, Huisingh CE, Bradley LA. 2014. Predictors of adherence to a brief behavioral insomnia intervention: daily process analysis. Behav Ther. 45(3):430-42. PMID: 24680236


    Herbert MS, Goodin BR, Pero ST 4th, Schmidt JK, Sotolongo A, Bulls HW, Glover TL, King CD, Sibille KT, Cruz-Almeida Y, Staud R, Fessler BJ, Bradley LA, Fillingim RB. 2014. Pain hypervigilance is associated with greater clinical pain severity and enhanced experimental pain sensitivity among adults with symptomatic knee osteoarthritis. Ann Behav Med. 48(1):50-60. PMID: 24352850  PMCID: PMC 4063898


    King CD, Sibille KT, Goodin BR, Cruz-Almeida Y, Glover TL, Bartley E, Riley JL,Herbert MS, Sotolongo A, Schmidt J, Fessler BJ, Redden DT, Staud R, Bradley LA, Fillingim RB. 2013. Experimental pain sensitivity differs as a function of clinical pain severity in symptomatic knee osteoarthritis. Osteoarthritis Cartilage 21: 1243-1252 PMCID: PMC3831366


    Goodin BR, Pham Q, Glover T, King C, Sibille KT, Cruz-Almeida Y, Staud R, Redden D, Bradley LA, Fillingim R. 2013. Perceived racial discrimination, but not mistrust of medical researchers, predicts the heat pain tolerance of African Americans with symptomatic knee osteoarthritis. Health Psychology, 32: 1117-1126. PMCID: PMC3943939


    Goodin BR, Glover TL, Sotolongo A, King CD, Sibille KT, Herbert MS, Cruz-Almeida Y, Sanden SH, Staud R, Redden DT, Bradley LA, Fillingim RB. 2013. The association of greater dispositional optimism with less endogenous pain facilitation is indirectly transmitted through lower levels of pain catastrophizing. J Pain. 14(2):126-35. PMCID: PMC3592576


    Herbert MS, Varley AL, Andreae SJ, Goodin BR, Bradley LA, Safford MM. 2013. The association of pain and HbA1c in a predominantly black sample of community-dwelling adults with diabetes: a cross-sectional analysis. Diabetic Med 30: 1466-1471 PMCID: PMC3935766


    Cruz-Almeida Y, King CD, Goodin BR, Sibille KT, Glover TL, Riley JL, Sotolongo A, Herbert MS, Schmidt J, Fessler BJ, Redden DT, Staud R, Bradley LA, Fillingim RB. 2013. Psychological profiles and pain characteristics of older adults with knee osteoarthritis. Arthritis Rheum (Arthritis Care Res)  65: 1786-1794 PMCID: PMC3922880



     

  • Bridges LouAnna Lois WatersEndowed Chair, Division of Clinical Immunology and Rheumatology
    Professor of Medicine
    Director, Division of Clinical Immunology & Rheumatology

    Address: 
     

    Shelby Building, Room 178C
    1825 University Boulevard
    35294-2182

    Administrative Associate: Paula Kiley
    Shelby Building, Room 178B
    1825 University Blvd.
    Birmingham, AL35294-2182
    Telephone:205-934-0897
    Fax: 205-934-1564
    Email: pfkiley@uabmc.edu 

     

    Education

    BS, Preprofessional Studies, University of Notre Dame, 1980
    MD,Louisiana State University School of Medicine, 1984
    PhD, University of Alabama at Birmingham, 1995
    Internship and Residency,Internal Medicine, University of Texas Medical Branch, Galveston 1984-1987
    Chief Residency, Internal Medicine, University of Texas Medical Branch, Galveston 1987-1988
    Fellowship, Clinical Immunology and Rheumatology, University of Alabama at Birmingham, 1988-1991

     

    Research Team

    Stephanie S. Ledbetter, MS Program Manager
    Keith Wanzeck   Lab Manager
    Jinyi Wang Research Associate
    Selena D. Luckett-Smith, RN Study Coordinator
    Laticia Woodruff, RN Study Coordinator
    Dongmei Sun, PhD Database Manager
    Vincent Laufer MD/PhD Student

     



     

    Research Description and Potential Projects for Trainees

    My earliest research interest, the role of B lymphocytes and autoantibodies in rheumatoid arthritis (RA), particularly immunoglobulin gene expression and antibody repertoires in synovial tissue, formed the basis of my PhD studies. In addition, my research has focused on identification of genetic influences on RA susceptibility and severity, particularly in African-Americans, and on autoantibodies and biomarkers of treatment response in RA. I have led several multicenter consortia, including the Consortium for the Longitudinal Evaluation of African-Americans with Rheumatoid Arthritis (CLEAR) Registry and Repository; the Biorepository of the Treatment of Early Aggressive RA (TEAR) Trial; and the Treatment Efficacy and Toxicity in RA Database and Repository (TETRAD).

     

    Publications

    Click here for a complete list of publications in PubMed.

     

    Active Research Projects

     

    Multidisciplinary Clinical Research Center

    As Director of UAB's Multidisciplinary Clinical Research Center (MCRC), funded by NIH P60 AR064172, I oversee a multidisciplinary program to promote research related to the causes, diagnoses, treatments and improved care of patients with arthritis and musculoskeletal diseases. The MCRC contains an Administrative Core, a Methodology Core (led by Xiangqin Cui, PhD, and David Redden, PhD of the UAB Department of Biostatistics, SOPH) and two research projects (see below).

    The mission of the MCRC Methodology Core is to develop and provide state of the art methodology and methodological education in the collaborative support of clinical and translational research in arthritis and musculoskeletal disease (MSD) at the local, regional, national, and international level. Toward this goal, the Core will continue to provide the statistical, epidemiological, outcomes research, statistical genetics, economics/cost effectiveness and bioinformatics leadership and expertise required to develop and perform cutting edge clinical research in arthritis and MSD it pursues four broad goals:

    • To support the design, data collection, management and analytic efforts of the MCRC projects
    • To nurture original research in methodology applicable to clinical research in arthritis and MSD
    • To develop new investigators in the area of arthritis and MSD research
    • To provide methodology seminars, workshops and mini-courses to introduce the newest methodological approaches to the MCRC research base.

    MCRC Project 1. Facilitating Treat-to-Target Strategies Using Novel Health Technology with Decision Support (PI: Jeffrey R. Curtis, MD, MS, MPH). This project will extend and evaluate novel health information technology to enable the systematic collection and integration of Patient Reported Outcome (PRO) and healthcare provider data in routine clinical practice; make use of this data to facilitate patient-provider interaction around optimal use of rheumatoid arthritis (RA) therapies; integrate this data with information in Electronic Health Record (EHR) systems; and demonstrate benefit for both process and outcomes among patients with RA.

    MCRC Project 2. Adaptive Immune Responses to Gut Microbiota in Juvenile and Adult Spondyloarthritis (PI: Charles O. Elson, MD, and Co-PI: Matthew Stoll, MD, PhD, MSCS). This project will integrate cutting-edge technologies of antigen identification with microbiome/metagenome analysis to provide novel information on the microbial contributions to spondyloarthritis. The data will result in new insights into the pathogenesis of SpA, suggest potential new biomarkers for diagnosis and monitoring, and lead to new approaches to therapy by manipulating the microbiota and adaptive immune responses to it.

     

    Center of Research Translation (CORT) in Gout and Hyperuricemia

    As Co-Director of the UAB CORT in Gout and Hyperuricemia (NIH P50 AR060772 - KG Saag, Contact PI; SL Bridges, Jr., PI), I am involved in three research projects focused on characterizing biomarkers of inflammation (CRP), vascular disease (endothelial function), and blood pressure changes associated with allopurinol (Project 1); examining factors associated with suboptimal gout care and factors influencing effective and safer dosing of allopurinol and colchicine in African-Americans and Caucasians (Project 2); and comparing the effectiveness of a novel pharmacy-based "virtual" Gout Clinic that includes protocol-driven care to usual care in the treatment of chronic gout (Project 3). The overall goal of our CORT (K. Saag, Director) is to improve the health of patients with gout and hyperuricemia by applying scientifically rigorous, state-of-the-art methodology to clinically important questions in translational investigation and to educate clinical investigators through an enrichment program. These innovative projects hold the promise of significant improvements in our understanding of the pathogenesis of gout and related co-morbid conditions, and may ultimately lead to better ways to predict, treat, or prevent gout and hyperuricemia.

     

    Rheumatic Disease Cores Center

    As Associate Director of the UAB Rheumatic Disease Cores Center (RDCC) (NIH P30 AR048311, John D Mountz, MD, PhD, PI and Director), I serve as collaborate with Dr. Mountz to provide assistance in the strategic planning, management and evaluation functions of the RDCC; and have primary responsibility for the development of Scientific Programs & Career Development program and for the management and monitoring the progress of the Pilot & Feasibility (P&F) Program. The RDCC consists of UAB investigators pursuing research in the rheumatic diseases, the Administrative Core, and three Research Cores: Comprehensive Flow Cytometry Core (CFCC); Analytical Imaging and Immunoreagent Core (AIIC); and Analytical Genomics and Transgenics Core (AGTC).

     

    VERVE Trial

    I serve as investigator and Director of the Biorepository for the Safety and Effectiveness of Live Zoster Vaccine in Anti-TNF Users (Varicella zostER VaccinE [VERVE]) trial, a randomized, double-blind, placebo-controlled large pragmatic trial to evaluate the immunogenicity, safety, and longer-term effectiveness of the live HZ vaccine in arthritis patients receiving anti-TNF therapy (UM1 AR065705 - JR Curtis, PI).

     

    TWEAK Trial

    A more recent interest is in mechanisms of muscle inflammation and it impact on mobility after joint replacement for arthritis. Though R01 HD084124 Overcoming TWEAK Signaling to Restore Muscle and Mobility after Joint Replacement (M Bamman, Contact PI/SL Bridges, Jr., MPI), we will test the hypothesis that progressive resistance exercise training plus adjunctive functional mobility training after total hip or knee arthroplasty will more effectively restore muscle mass and mobility function to healthy standards than usual care, particularly in patients with TWEAK (TNF-like weak inducer of apoptosis)-mediated muscle inflammation. We will perform a randomized controlled trial of THA/TKA patients to test this hypothesis and study the cellular and molecular mechanisms of muscle mass regulation.

     

    National Resource Center for High-Impact Clinical Trials in Medical Rehabilitation

    Our NIH-funded P2C National Resource Center for High-Impact Clinical Trials in Medical Rehabilitation (High-Impact Trials Center, HITC) will serve as a catalyst for the design and implementation of rigorous, high-impact clinical trials to advance medical rehabilitation research. Oversight of the Center is provided by Marcas Bamman, PhD (Director). I serve on the Executive Committee and as Director of the HITC Pilot Component (Pilot-C). The goal of this component is to catalyze the success of medical rehabilitation researchers and interdisciplinary teams by providing consultation, seed funds, key expertise and resources, and ultimately feedback, to medical rehabilitation researchers for the conduct of innovative pilot projects, early-stage proof-of-concept studies, and futility studies needed to shape more definitive clinical trials. The central goal will be met by achieving the following aims: Aim 1. To work closely with the Collaborative Component, providing consultation to medical rehabilitation research teams on how to: 1) Formulate and refine strong and impactful research questions; 2) Identify the goals and aims needed to achieve future clinical outcome trials. Aim 2. To identify and prioritize the most competitive proposals for both pilot studies and voucher funding via an annual peer review process. Aim 3. To provide expertise, resources, and/or mentorship to selected pilot study awardees with ongoing availability during the planning and implementation phases in order to: 1) Bolster the scientific yield of each pilot study; and 2) Position each awardee for a subsequent, highly competitive clinical trial application. Aim 4. To provide constructive and substantive feedback to applicants not selected for funding, and to direct those applicants toward other programs and opportunities within the Center that can strengthen future applications. The Pilot-C will award four $40K pilot studies per year.

     

    The Rheumatoid Arthritis Synovial Tissue Network

    I served as site PI of the Rheumatoid Arthritis Synovial Tissue Network (REASON) Study (UH2 AR067687 - RM Pope, Northwestern Univ). The goals of this study are to create a new generation of rheumatologists in the United States who will perform minimally invasive ultrasound guided synovial biopsies that is critical for obtaining of synovial tissue from patients at all phases of RA (early, established, DMARD or biologic inadequate response). We have assembled a consortium of leading academic rheumatology groups which includes UAB, Columbia University, Mayo Clinic, Washington University, University of Michigan, and Northwestern University to obtain synovial tissue from RA patients for translational studies to identify novel pathways and potential biomarkers that might predict therapeutic response. We anticipate that we will be part of the NIH Accelerating Medicines Partnership to provide training for synovial biopsy, as well as RA synovial tissue samples to the collaborative research network.

     

  • ChathamProfessor of Medicine
    Louis W. Heck Clinical Scholar
    Clinical Director, Division of Clinical Immunology & Rheumatology

     

    Address:

    Faculty Office Tower (FOT), Room 858
    510 20th Street South
    35294-3408

    Telephone:(205) 996-5602
    Email:wchatham@uab.edu

     

    Education

    BSE, Biomedical Engineering, Duke University, 1976
    MD,Vanderbilt University, 1980
    Internship and Residency,Internal Medicine, University of North Carolina Hospital, Chapel Hill, NC, 1980-1983
    Fellowship,Rheumatology, University of Alabama at Birmingham, 1986-1989

     

    Clinical Interests

    • Lupus
    • Immunodeficiency-associated rheumatic disease
    • Sarcoidosis
    • Auto-inflammatory and macrophage activation syndromes

     

    Research Description

    Dr. Chatham's research program is focused on the biology of TNF family receptors and their ligands (including BLyS/BAFF) as these relate to disease expression in lupus and other inflammatory/autoimmune disorders. The therapeutic implication of these studies has been extended to current clinical studies that involve the use of monoclonal reagents and soluble receptors targeting BlyS/BAFF in patients with active systemic  lupus as well as their potential use in autoimmunity associated with immunodeficiency. Additional collaborative studies are examining the biology of type-1 interferons and  interferon-alpha blocking reagents on disease activity in systemic lupus and macrophage activation disorders.

     

    Publications

    Click here for a more complete list of publications. Below are a few selected papers.


    Chatham W, Chadha A, Fettiplace J, Kleoudis C, Bass D, Roth D, Gordon D.2017. A randomized, open-label study to investigate the effect of belimumab on pneumococcal vaccination in patients with active, autoantibody-positive systemic lupus erythematosus. Lupus. 2017, Jan 1 [Epub ahead of print] PMID: 28467293


    Cron RQ, Chatham WW. 2016. Development of spondyloarthropathy following episodes of macrophage activation syndrome in children with heterozygous mutations in haemophagocytic lymphohistiocytosis-associated genes. Clin Exp Rheumatol. 34(5):953. PMID: 27383696


    Zhang M, Bracaglia C, Prencipe G, Bemrich-Stolz CJ, Beukelman T, Dimmitt RA, Chatham WW, Zhang K, Li H, Walter MR, De Benedetti F, Grom AA, Cron RQ. 2016. A Heterozygous RAB27A Mutation Associated with Delayed Cytolytic Granule Polarization and Hemophagocytic Lymphohistiocytosis.J Immunol. 196(6):2492-503 PMC4779709


    Stohl W, Hiepe F, Latinis KM, Thomas M, Scheinberg MA, Clarke A, Aranow C, Wellborne FR, Abud-Mendoza C, Hough DR, Pineda L, Migone TS, Zhong ZJ, Freimuth WW, Chatham WW; BLISS-52 Study Group; BLISS-76 Study Group. 2012. Belimumab reduces autoantibodies, normalizes low complement levels, and reduces select B cell populations in patients with systemic lupus erythematosus. Arthritis Rheum. 64(7):2328-37. PMID:22275291 PMCID:PMC3350827


    Furie R, Petri M, Zamani O, Cervera R, Wallace DJ, Tegzová D, Sanchez-Guerrero J, Schwarting A, Merrill JT, Chatham WW, Stohl W, Ginzler EM, Hough DR, Zhong ZJ, Freimuth W, van Vollenhoven RF; BLISS-76 Study Group. 2011. A phase III, randomized, placebo-controlled study of belimumab, a monoclonal antibody that inhibits B lymphocyte stimulator, in patients with systemic lupus erythematosus. Arthritis Rheum. 63(12):3918-30. PMID:22127708

     

  • Curtis2013Harbert Ball Endowed Chair Professor 
    Director, UAB Arthritis Clinical Intervention Program
    Co-Director, UAB Center for Education and Research on Therapeutics (CERTS) of Musculoskeletal Disorders
    Co-Director, UAB PharmacoEpidEmiology and phaRmcoeconomics (PEER) Unit
    University of Alabama at Birmingham, Division of Clinical Immunology and Rheumatology

     

    Address:

    Faculty Offices Tower, room 802
    510 20th Street South
    Birmingham, AL 35294

    Telephone:(205) 975-2176
    Email:jcurtis@uab.edu

     

    Education

    BS (Biology),University of California at San Diego
    MD,Oregon Health & Sciences University, Portland, OR
    MPH,Oregon Health & Sciences University, Portland, OR
    Residency (Internal Medicine):Oregon Health & Science University
    Fellowship (Clinical Immunology and Rheumatology): University of Alabama at Birmingham
    MS (Epidemiology), Harvard School of Public Health
    Postdoctoral (Clinical Informatics):Stanford University

     

    Research and Clinical Interests

    Dr. Jeffrey Curtis is a Professor of Medicine in the Division of Clinical Immunology and Rheumatology at the University of Alabama at Birmingham (UAB). Dr. Curtis received a Medical Degree (MD) and a Master of Public Health (MPH) degree from Oregon Health & Sciences University in Portland, OR. He subsequently completed a residency in internal medicine at Oregon Health & Science University and a fellowship in rheumatology at UAB. He completed a graduate program in Clinical Informatics at Stanford University and received his Master of Science (MS) degree in epidemiology at the Harvard School of Public Health. He is board certified in both rheumatology and clinical informatics.

    Dr. Curtis currently holds the William J. Koopman Endowed Professorship in Rheumatology and Immunology at UAB. He is the Co-Director of the UAB Center for Education and Research on Therapeutics (CERTs) of Musculoskeletal Disorders, which has a major emphasis on evaluating the safety and comparative effectiveness of medications for rheumatic diseases. Additionally, as the Director of the UAB Arthritis Clinical Intervention Program, he leads the clinical trials unit for the rheumatology division at UAB, with a particular focus on rheumatoid arthritis (RA) and psoriatic arthritis (PsA). He is the Co-Director of the UAB Pharmacoepidemiology and Pharmacoeconomics Research (PEER) Unit. PEER uses multiple large data sources to study comparative effectiveness questions across multiple chronic diseases. These data sources include national administrative data from Medicare and commercial health plans, electronic health record data, and large registries. In 2012, he was awarded the Henry Kunkel Young Investigator Award by the American College of Rheumatology (ACR) and was accepted into the American Society for Clinical Investigation (ASCI) in 2016.

    The evaluation of the efficacy, comparative effectiveness, and safety of the medications used to treat rheumatoid arthritis and spondyloarthritis are among Dr. Curtis’s research interests. He served on the Core Expert Panel for the ACR’s 2008, 2012, and 2015 Recommendations for the Use of Nonbiologic and Biologic Disease Modifying Antirheumatic Drugs in RA. He was the Deputy Director for a collaborative project between the FDA, the Agency for Healthcare Research and Quality (AHRQ), and a number of academic centers studying the safety of biologic agents using multiple, pooled national data sources. He is the Co-PI of the PCORI-funded Patient Powered Research Network “Arthritis-Power” registry, focused on RA, psoriasis, and psoriatic arthritis. He also leads the multi-center NIH-funded large pragmatic randomized controlled trial “VERVE” studying the safety and effectiveness of the live herpes zoster vaccine in patients receiving biologic agents. He is a member of the Center for Disease Control (CDC) Advisory Committee on Immunization Practices (ACIP) Herpes Zoster workgroup. In 2015, he was appointed as a member to the FDA Arthritis Advisory Committee.

    Dr. Curtis also studies risk factors for and outcomes of osteoporosis. He was a member of the ACR’s task force to update recommendations for the management of glucocorticoid induced osteoporosis (GIOP). He served on the ASBMR Task Force on Atypical Subtrochanteric and Diaphyseal Fractures.

    Dr. Curtis is a member of the American College of Rheumatology (ACR), the International Society for Pharmacoepidemiology (ISPE), the American Medical Informatics Association (AMIA), and the American Society of Bone and Mineral Research (ASBMR). He has been on the editorial board for Arthritis & Rheumatism, Pharmacoepidemiology and Drug Safety (PDS) and Arthritis Care and Research (AC&R). He has authored more than 350 peer-reviewed manuscripts, review articles and book chapters.

     

    Publications

    Click here for a complete list of publications. Below are a few selected papers.


    Curtis JR, McVie T, Mikuls T, Reynolds, RJ, Navarro I, O’Dell J, Moreland L, Bridges SL, Ranganath, VK, Cofield SS. 2013. Clinical Response with 12 Weeks as a Predictor of Future Low Disease Activity in Early Rheumatoid Arthritis Patients: Results from the TEAR Trial. Journal of Rheumatology. PMID 23588939; PMC 3694569


    Curtis JR, Xie F, Chen L, Muntner P, Grijalva CG, Spettell C, Fernandes J, McMahan RM, Baddley JW, Saag KG, Beukelman T, Delzell E. 2012. Use of a disease risk score to compare serious infections associated with anti-tumor necrosis factor therapy among high- versus lower-risk rheumatoid arthritis patients. Arthritis Care Res (Hoboken). 64(10):1480-9. PMID: 22833479 PMC3687540


    Zhang J, Xie F, Delzell E, Chen L, Winthrop KL, Lewis JD, Saag KG, Baddley JW, Curtis JR. 2012. Association between vaccination for herpes zoster and risk of herpes zoster infection among older patients with selected immune-mediated diseases. JAMA. 308(1):43-9. PMID: 22760290


    Curtis JR, van der Helm-van Mil AH, Knevel R, Huizinga TW, Haney DJ, Shen Y, Ramanujan S, Cavet G, Centola M, Hesterberg LK, Chernoff D, Ford K, Shadick NA, Hamburger M, Fleischmann R, Keystone E, Weinblatt ME. 2012. Validation of a novel multibiomarker test to assess rheumatoid arthritis disease activity. Arthritis Care Res (Hoboken). 64(12):1794-803. PMID: 22736476


    Grijalva CG, Chen L, Delzell E, Baddley JW, Beukelman T, Winthrop KL, Griffin MR, Herrinton LJ, Liu L, Ouellet-Hellstrom R, Patkar NM, Solomon DH, Lewis JD, Xie F, Saag KG, Curtis JR. 2011. Initiation of tumor necrosis factor-α antagonists and the risk of hospitalization for infection in patients with autoimmune diseases. JAMA. 306(21):2331-9. PMC3428224

     

     

  • Sam Dalvi 16Assistant Professor of Medicine

    Division of Clinical Immunology and Rheumatology

    Address:

    Faculty Offices Tower (FOT)
    510 20th Street South
    Birmingham, AL35294

    Telephone: (205) 996-5602

     

    Education:

    B.S./B.A.: Auburn University, 2001
    M.D.: University of Alabama at Birmingham, 2005
    Internship:University of Alabama at Birmingham, 2006
    Residency:University of Alabama at Birmingham, 2008
    Fellowship: New York University Hospital for Joint Diseases, 2012

     

    Research Interests

    Dr. Dalvi’s research interests involve the role of environmental stimuli in the development of autoimmunity as well as the role of lead toxicity and gouty arthritis. In addition, he is planning to develop a vasculitis registry to investigate potential markers of disease activity in patients with vasculitis.

     

    Clinical Interests

    Dr. Dalvi’s main clinical interests include the following: Giant cell/temporal arteritis, Takayasu’s arteritis, polymyalgia rheumatic (PMR), Granulomatosis with polyangiitis (Wegener’s disease), Microscopic polyangiitis, Eosinophilic granulomatosis with polyangiitis (Churg-Strauss disease), Polyarteritis nodosa (PAN), cutaneous vasculitis, cryoglobulinemic syndromes, drug-induced vasculitis..

    He also has a strong clinical interest in the following conditions:

    Rheumatoid arthritis
    Osteoarthritis
    Gout
    Pseudogout (CPPD)
    Systemic Lupus Erythematosus
    Psoriatic arthritis
    Ankylosing spondylitis
    Dermatomyositis
    Polymyositis

    Antiphospholipid antibody syndrome
    Behcet’s syndrome
    Sarcoidosis
    Scleroderma
    Sjogren’s syndrome
    Relapsing Polychondritis

     

    Publications


    Dalvi, SR, Moser, DW; Samuels, J. 2013. Ultrasound and Treatment Algorithms of RA and JIA. Rheumatic Disease Clinics of North America. 39(3):669-88). PMID: 23719081

    Dalvi, SR, Pillinger, MH. 2013. Saturnine gout, redux: a review. American Journal of Medicine. 126:450.e1-450.e8. PMID: 23510947

    Dalvi, SR, Yildirim, R; Santoriello, D; Belmont, HM. 2012. Pseudo-pseudo Meigs' syndrome in a patient with systemic lupus erythematosus. Lupus. 21:1463-1466. PMID: 22983642

    Dalvi, SR, Yildirim, R; Yazici, Y. 2012. Behcet's Syndrome. Drugs. 72:2223-2241. PMID: 23153327

     

     

  • Danila 2017Associate Professor of Medicine
    Ambulatory Clinical Director, Rheumatology

    Address: 
     

    Faculty Office Tower, room 838
    510 20th Street South, Birmingham, AL 35294-3408

    Patient care telephone: (205) 996-7438
    Patient care fax: (205) 583-8060
    Email: mdanila@uab.edu

    Administrative Assistant:
    Patricia Taylor
    Telephone: (205) 996-5602
    Fax: (205) 934-4198

    Education

    MD,“Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania
    Internship (General Medicine),“Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania
    MSc (Microbiology),University of Victoria, Victoria, BC, Canada
    Residency in Internal Medicine,University of Illinois at Chicago-Advocate Christ Medical Center, Oak Lawn, IL
    Clinical Rheumatology Fellow, University of Alabama at Birmingham
    MSPH (Epidemiology), School of Public Health, University of Alabama at Birmingham
    Graduate Certificate in Health Quality and Safety, School of Health Professions, University of Alabama at Birmingham

     
    Clinical Interests

    • Rheumatoid Arthritis
    • Connective tissue associated interstitial lung disease
    • Sjogren's syndrome
    • Scleroderma

     

    Research Interests

    Dr. Danila is an Associate Professor of Medicine in the Division of Clinical Immunology and Rheumatology at the University of Alabama at Birmingham (UAB). Dr. Danila is an implementation scientist and outcome researcher, passionate about improving the quality, effectiveness and processes/delivery of medical care for patients. Her research program focuses on two main areas: i) the design and evaluation of culturally-adapted and literacy-appropriate health care interventions that improve outcomes for patients with chronic conditions; and ii) the development and implementation of strategies to assist physicians and other health care professionals in engaging in shared decision making and evidence-based clinical practice.

    Dr. Danila is also interested in the redesign of healthcare delivery processes, decreasing healthcare costs and increasing value-based medical care. She has been actively involved as volunteer for the American College of Rheumatology (ACR). She served on the ACR Insurance Subcommittee (ISC) from 2012-2016.

     

    Publications

    Click here for a list of publications.

     



  • jeffrey_edbergProfessor of Medicine
    Co-Director, Participant & Clinical Interactions Resources (PCIR)

     

    Address:

    Shelby Building, Room 207
    1825 University Boulevard
    35294-2182

    Telephone:(205) 934-0894
    Email: jedberg@uab.edu

     

    Education

    BS (Chemistry), University of Illinois, 1986
    PhD, University of Virginia, 1990
    Post-Doctoral Training, Cornell University medical College, 1988-1991

     

    Research Description

    Wegener's granulomatosis, an anti-neutrophil cytoplasmic antibody (ANCA)-positive systemic small vessel vasculitide, is characterized by inflammatory lesions with granuloma formation in the upper and lower airways, pauci-immune glomerulonephritis, and anti-proteinase 3 autoantibodies. Although Wegener's granulomatosis is considered idiopathic, there has been substantial interest in environmental factors as either etiologic or accelerating risk factors, with Staphylococcus aureus having attracted substantial attention as one such environmental factor. Although consensus about etiology remains elusive, the nature of the host response has emerged as an important determinant for disease phenotype and severity. Although Wegener's granulomatosis occurs sporadically, and does not show classical familial clustering and transmission characteristic of some autoimmune diseases, the identification of important genetic factors in Wegener's granulomatosis is not only feasible but also potentially very fruitful in providing insights into pathogenesis and potential therapeutic targets. Building on the clinical trial of etanercept in Wegener's granulomatosis, Dr. Edberg, in collaboration with Drs. Kimberly and Kaslow, is developing a renewable genetic repository to explore the relationship between the Wegener's granulomatosis diathesis and genetic polymorphisms in candidate molecules, selected for their role in pathophysiology. These studies also will involve identification of new polymorphisms in such molecules and application of these to this cohort.

     

    Publications

    Click here for a more complete list of publications. Below are a few selected papers.


    Li X, Baskin JG, Mangan EK, Su K, Gibson AW, Ji C, Edberg JC, Kimberly RP. The unique cytoplasmic domain of human FcγRIIIA regulates receptor-mediated function. 2012. J Immunol. 189(9):4284-94. PMID:23024279


    Kelley JM, Monach PA, Ji C, Zhou Y, Wu J, Tanaka S, Mahr AD, Johnson S, McAlear C, Cuthbertson D, Carette S, Davis JC Jr, Dellaripa PF, Hoffman GS, Khalidi N, Langford CA, Seo P, St Clair EW, Specks U, Stone JH, Spiera RF, Ytterberg SR, Merkel PA, Edberg JC, Kimberly RP. 2011. IgA and IgG antineutrophil cytoplasmic antibody engagement of Fc receptor genetic variants influences granulomatosis with polyangiitis. Proc Natl Acad Sci U S A. 108(51):20736-41. PMID:22147912


    Perkins EA, Landis D, Causey ZL, Edberg Y, Reynolds RJ, Hughes LB, Gregersen PK, Kimberly RP, Edberg JC, Bridges SL Jr; Consortium for the Longitudinal Evaluation of African Americans with Early Rheumatoid Arthritis Investigators. 2012. Association of single-nucleotide polymorphisms in CCR6, TAGAP, and TNFAIP3 with rheumatoid arthritis in African Americans. Arthritis Rheum. 64(5):1355-8. PMID:22127930


    Tan W, Sunahori K, Zhao J, Deng Y, Kaufman KM, Kelly JA, Langefeld CD, Williams AH, Comeau ME, Ziegler JT, Marion MC, Bae SC, Hyun Lee J, Lee JS, Chang DM, Wook Song Y, Yu CY, Kimberly RP, Edberg JC, Brown EE, Petri MA, Ramsey-Goldman R, Vilá LM, Reveille JD, Alarcón-Riquelme ME, Harley JB, Boackle SA, Stevens AM, Hal Scofield R, Merrill JT, Freedman BI, Anaya JM, Criswell LA, Jacob CO, Vyse TJ, Niewold TB, Gaffney PM, Moser KL, Gilkeson GS, Kamen DL, James JA, Grossman JM, Hahn BH, Tsokos GC, Tsao BP; on behalf of the BIOLUPUS GENLES networks. 2011. Association of PPP2CA polymorphisms with SLE susceptibility in multiple ethnic groups. Arthritis Rheum.  63(9):2755-63 PMID: 21590681

     

  • Elgavish2rev2Associate Professor of Medicine
    Program Manager, Program in Immunology

     
    Address: 

    Shelby Building, Room 415
    1825 University Boulevard
    35294-2182

    Telephone:(205) 934-6547
    Email:aelgavis@uab.edu

     

    Education

    BS, Tel Aviv University, Tel Aviv, Israel
    MSc,Tel Aviv University, Tel Aviv, Israel
    PhD, Wezimann Institute of Science, Rehovoth, Israel
    Fogarty Visiting Fellow, Laboratory of Membrane Biology, NIH

     

    Awards

    Fogarty Fellowship, NIH, 1979-1981

    American Lung Association, Career Investigator Award, 1987-1992

     

    Research Interests

    My main scientific interests have been in the biology of the genitourinary tract. Bladder Pain Syndrome/Interstitial Cystitis (BPS/IC) is a chronic inflammatory disease of the bladder wall. More than 100 years after first being described, the diagnosis of BPS/IC is still associated with controversy. Given the difficulties associated with the diagnosis of BPS/IC, it is not surprising that the etiology of this syndrome is poorly understood. Several theories for the etiology of BPS/IC have been proposed over the years including infection, immunological etiology, leaky urothelium resulting from a deficiency of its surface coat of glycosaminoglycans, activated mast cells and neural changes.

    In vitro studies in my laboratory have been consistent with the possibility that BPS/IC may develop in response to noxious stimuli in the bladder lumen. Thus, lipoteichoic acid (LT-2), a cell wall component of the gram-positive bacterium Streptococcus faecalis, stimulated the proliferation rate of a subpopulation of basal uroepithelial cells with high proliferative potential (possibly stem cells). their progeny differentiated at a higher rate and displayed abnormal expression and cellular distribution of β1 integrins, and LT-2 required activation of iNOS and NFκB. Moreover, our studies provided evidence for altered proliferative ability of progenitors of urothelial cells in cell cultures isolated from patients with BPS/IC. These studies raised a number of questions: What are the mechanisms by which noxious stimuli in the bladder lumen may trigger abnormal function of the muscle and nerve tissue underlying the uroepithelium, causing pain and persistent urge to void? In addition, how is it possible that chronic symptoms similar to those characteristic of bacterial cystitis persist for years in patients with BPS/IC in whom no infectious agent is detected at the time of diagnosis? Based on emerging data from several laboratories, I postulated in a recent review that epigenetic reprogramming mechanisms in the bladder may provide an explanation for uroepithelial, mast cells and nerve cell abnormalities in BPS/IC, as well as propagation of this altered state in the absence of the signal that may have triggered it. Data supporting this hypothesis would provide a rationale for new diagnostic, treatment and dietary intervention options for BPS/IC.

    My second scientific interest is dietary prevention of prostate cancer (PC). PC is the most commonly diagnosed cancer in North American men. Findings of latent or clinically insignificant PC occurs in a large proportion, and at equal rates, in autopsy studies among men from Asian countries and the United States. In contrast, the incidence of clinically significant PC is an order of magnitude higher in the United States. Epidemiological studies suggest that this might be attributable to differences in environmental factors and life style, including nutrition. Aggressive PC is less prevalent among Asian men where the intake of soy products is very high. However, with Westernization and loss of traditional eating habits, the pattern of disease incidence is also changing in Asian men. On the basis of these findings, it has been postulated that phytoestrogens, including genistein, may have a preventive role in PC. Studies in my laboratory in a transgenic mouse model of prostate cancer (TRAMP mice), supported this hypothesis

    Prostate cancer fatalities are rarely due to primary tumors, but rather to widespread metastatic disease. The preferential colonization of bone by prostatic adenocarcinomas has been attributed to the passage of prostate epithelial cells from the prostate to the spine via paravertebral blood vessels. However, molecular mechanisms that facilitate retention of metastatic cells in bone and, their subsequent unrestricted proliferation, are poorly understood. In my laboratory, in vitro studies in cell cultures isolated from the human prostate and in vivo studies in the  transgenic mouse model of prostate cancer focused on cell adhesion-mediated molecular mechanisms that: (i) May underlie progression of slow growing prostate tumors to metastatic growth; and that (ii) May be the target of preventive strategies that delay progression of indolent prostate tumors to metastatic growth.

    More recent collaborative studies with Gabriel A. Elgavish were focused on developing an MRI method for early noninvasive detection of developing PC.

    In the past few years, in collaborative studies with Harry W. Schroeder, Jr., my interests have expanded to the link between natural protection, e.g., against pneumococci, and D(H) gene conservation.

     

    Publications

    Click here for a complete list of publications. Below are a few selected papers


    Mohamed Khass, Robert L. Schelonka, Cun Ren Liu, Ada Elgavish, Laurence Morel, Peter D. Burrows, Harry W. Schroeder, Jr. 2017. Alterations in B cell development, CDR-H3 repertoire and dsDNA-binding antibody production among C57BL/6 ΔD−iD mice congenic for the lupus susceptibility loci sle1, sle2 or sle3. Autoimmunity 50: 42-51.


    Wang Y, Hwangpo T, Martin MP, Vince N, Qi Y, Reynolds RJ 4th, Absher D, Gao X, Ballinger CA, Burrows PD, Atkinson TP, Brown EE, Elgavish A, Liu C, Carrington M, Schroeder HW. 2016. Killer cell immunoglobulin-like receptors are associated with common variable immune deficiency pathogenesis. J Allergy Clin Immunol. 138(5):1495-1498. PMID: 27665490


    Yuge Wang, Pratibha Kapoor, Robert Parks, Aaron Silva-Sanchez, S. Munir Alam, Laurent Verkoczy, Hua-Xin Liao, Yingxin Zhuang, Peter Burrows, Michael Levinson, Ada Elgavish, Xiangqin Cui, Barton F. Haynes and Harry Schroeder Jr. 2016. HIV-1 gp140 epitope recognition is influenced by immunoglobulin DH gene segment sequence. Immunogenetics. 68(2):145-55. PMID: 26687685 PMCID: PMC4729650


    Silva-Sanchez A, Liu CR, Vale AM, Khass M, Kapoor P, Elgavish A, Ivanov II, Ippolito GC, Schelonka RL, Schoeb TR, Burrows PD, Schroeder HW Jr. 2015. Violation of an Evolutionarily Conserved Immunoglobulin Diversity Gene Sequence Preference Promotes Production of dsDNA-Specific IgG Antibodies. PLoS One. 10(2):e0118171. PMID: 25706374 PMCID: PMC4338297


    Vale AM, Kapoor P, Skibinski GA, Elgavish A, Mahmoud TI, Zemlin C, Zemlin M, Burrows PD, Nobrega A, Kearney JF, Briles DE, Schroeder HW Jr. 2013. The link between antibodies to OxLDL and natural protection against pneumococci depends on D(H) gene conservation. J Exp Med. 210(5):875-90. PMID: 23589567 PMCID: PMC3646500

  • Gaffo Oct2015Associate Professor of Medicine
    Associate Director, Rheumatology Fellowship Training Program
    Rheumatology Section Chief, Birmingham VA Medical Center

     

    Address:

    Shelby Bldg., room 306
    35294

    Telephone:(205) 975-8909
    Email:agaffo@uabmc.edu

     

    Education

    MD:Universidad Peruana Cayetano Heredia, 1991-1999, Lima, Peru 
    Residency: Internal Medicine, University of Alabama at Birmingham, 2002-2005
    Fellowships:

    Rheumatology, University of Alabama at Birmingham, 2005-2007
    Quality Improvement, National VA Quality Scholars Program at the Birmingham VA Medical Center, 2007-2009

    Postgraduate:MSPH in Epidemiology, University of Alabama at Birmingham School of Public Health, 2006-2008)

     

    Clinical Interests

    • General Rheumatology Practice with emphasis in connective tissue diseases and metabolic crystal disorders.
    • Quality improvement in musculoskeletal disease.
    • Care of patients with vasculitis

     

    Research interests

    • Epidemiology of hyperuricemia and gout, with focus on their association with ethnic, dietary, and cardiovascular factors
    • Quality of care in arthritis and rheumatic diseases
    • Clinical and therapeutic aspects of vasculitis care

     

    Publications

    Click here for a more complete list of publications. Below are selected papers


    Sattui SE, Singh JA, Gaffo AL. 2014. Comorbidities in patients with crystal diseases and hyperuricemia. Rheum Dis Clin North Am. 40(2):251-78. PMID: 24703346 PMCID: PMC4159668


    Gaffo AL, Jacobs DR Jr, Sijtsma F, Lewis CE, Mikuls TR, Saag KG. 2012. Serum urate association with hypertension in young adults: analysis from the Coronary Artery Risk Development in Young Adults cohort. Ann Rheum Dis. 2012 Sep 14. [Epub ahead of print]PMID:22984170


    Gaffo AL, Jacobs DR Jr, Lewis CE, Mikuls TR, Saag KG. 2012. Association between being African-American, serum urate levels and the risk of developing hyperuricemia: findings from the Coronary Artery Risk Development in Young Adults cohort. Arthritis Res Ther. 14(1):R4. PMID:22225548


    Gaffo AL, Schumacher HR, Saag KG, Taylor WJ, Dinnella J, Outman R, Chen L, Dalbeth N, Sivera F, Vázquez-Mellado J, Chou CT, Zeng X, Perez-Ruiz F, Kowalski SC, Goldenstein-Schainberg C, Chen L, Bardin T, Singh JA. 2012. Developing a provisional definition of flare in patients with established gout. Arthritis Rheum. 64(5):1508-17. PMID:22083456

     

     

  • Gibson_2012Assistant Professor of Medicine

     

    Address:

    Shelby Bldg, Room 203
    1825 University Blvd.
    35294

    Telephone:(205) 975-6407

    Fax:(205) 996-6734
    Email:gibsona@uab.edu

     

    Education

    BS (Biology), City University of New York, Brooklyn College, 1984
    PhD (Genetics), City University of New York, Graduate School, 1995
    MBA, American Intercontinental, Atlanta,GA, 2003
    Postdoctoral Training, Cornell University Medical College/Hospital for Special Surgery, 1995-1996
    Postdoctoral Training, University of Alabama at Birmingham, 1996-1999

     

    Research Interests:

    Molecular genetics and epigenetics of autoimmune diseases: Characterization of genetic variants on the SLE-linked q21-q42 region of chromosome 1; Structure and function of Fc gamma receptors in inflammation.

     

    Publications

    Click here for a more complete list of publications. Below are a few selected papers.


    Shah S, Gibson AW, Ji C, Darrington E, Mobley J, Kojima K, Edberg JC, Kimberly RP. 2016. Regulation of FcRγ function by site-specific serine phosphorylation. J Leukoc Biol. 101(2):421-428. PMID: 27630214 PMCID: PMC5235907


    Li X, Gibson AW, Kimberly RP. 2014. Human FcR polymorphism and disease. Curr Top Microbiol Immunol. 382:275-302. PMID: 25116105.


    Absher DM, Li X, Waite LL, Gibson A, Roberts K, Edberg J, Chatham WW, Kimberly RP. 2013. Genome-wide DNA methylation analysis of systemic lupus erythematosus reveals persistent hypomethylation of interferon genes and compositional changes to CD4+ T-cell populations. PLoS Genet. 9(8):e1003678. PMID: 23950730 PMCID: PMC3738443

    Gibson AW, Li X, Wu J, Baskin JG, Raman C, Edberg JC, Kimberly RP. 2012. Serine phosphorylation of FcγRI cytoplasmic domain directs lipid raft localization and interaction with protein 4.1G. J Leukoc Biol. 91(1):97-103. PMID:22003208. Free PMC Article

    Gibson AW, Li FJ, Wu J, Edberg JC, Su K, Cafardi J, Wiener H, Tiwari H, Kimberly RP, Davis RS. 2009. The FCRL3 -169CT promoter single-nucleotide polymorphism, which is associated with systemic lupus erythematosus in a Japanese population, predicts expression of receptor protein on CD19+B cells. Arthritis Rheum. 60(11):3510-2.  PMID: 19877046

  • Beatriz Hanaoka 2016 BAssistant Professor of Medicine

    Division of Clinical Immunology and Rheumatology

    Address:

    Shelby Building, Room 210
    1825 University Boulevard
    35294

    Telephone: (205) 930-8347

    Fax: (205) 930-8340

    Email: bhanaoka@uabmc.edu

     

    Education:

    M.D. University of Sao Paulo, Brazil, 2005
    Residency: (Internal Medicine), Cleveland Clinic Foundation, Cleveland, OH, 2005-2008
    Fellowship: (Rheumatology) Columbia University, NY, 2008-2010

     

    Research Interests

    Dr. Hanaoka is conducting clinical studies to understand the reasons behind the decline in skeletal muscle function and physical activity in patients with rheumatic diseases, particularly in rheumatoid arthritis (RA). Her research is primarily focused on understanding at a mechanistic level the metabolic and physiologic abnormalities of skeletal muscle in RA patients. More specifically, she is investigating if insulin resistance is an underlying cause of skeletal muscle dysfunction in RA patients by conducting clinical trials utilizing an insulin sensitizer. This research is being supported by a K23 NIAMS patient-oriented career development award.

    Dr. Hanaoka is also conducting additional collaborative studies with her husband, Dr. Prabha Nagareddy (UAB - Nutrition Sciences), and Dr. Andrew Murphy (Baker IDI Institute, Melbourne, Australia) to examine the molecular pathways that contribute to increased cardiovascular disease risk in RA patients.

     

    Publications

    Click here for a more complete list of publications. Below are selected papers

    Cleary LC, Crofford LJ, Long D, Charnigo R, Clasey J, Beaman F, Jenkins KA, Fraser N, Srinivas A, Dhaon N, Hanaoka BY. 2015. CT based muscle density predicts muscle function and health-related quality of life in patients with idiopathic inflammatory myopathies. Arthritis Care Res. 67(7):1031-40. PMID: 25623494

    Hanaoka BY, Cleary LC, Long DE, Srinivas A, Jenkins KA, Bush HM, Starnes CP, Rutledge M, Duan J, Fan Q, Fraser N, Crofford LJ. 2015. Physical impairment in patients with idiopathic inflammatory myopathies is associated with the American College of Rheumatology functional status measure. Clinical Rheumatology. 34(11);1929-37. PMID: 25388646

    Hanaoka BY, Peterson CA, Crofford LJ. 2012. Glucocorticoid effects on skeletal muscle: benefit and risk in patients with autoimmune inflammatory rheumatoid diseases. Expert Review in Clinical Immunology. 8(8):695-7. PMID: 23167679

    Hanaoka BY, Peterson CA, Horbinski C, Crofford LJ. 2012. Implications of glucocorticoid therapy in idiopathic inflammatory myopathies. Nat. Rev. Rheumatol. 8: 448-457. PMID: 22688888

     

  • Hsu 2017Associate Professor of Medicine

    Address:

    Shelby Building, Room 311
    1825 University Boulevard
    35294-2182

     

    Telephone:(205) 934-8909
    Fax: 205-975-6648
    Email: rheu078@uab.edu

    Dr. Hsu's webpage in the School of Medicine

     

    Education

    BS, Chinese Culture University, Taipei, Taiwan, 1986
    MS,Rutgers University, New Brunswick, NJ, 1990
    PhD,Rutgers University, New Brunswick, NJ, 1995
    Postdoctoral Fellow,University of Alabama at Birmingham, 1999

     

    Research Description

    We have identified that autoimmune BXD2 mice exhibit unique features, including spontaneous formation of germinal centers, increased expression of activation-induced cytidine deaminase (AID), increased production of pathogenic autoantibodies that are polyreactive, significantly increased percentage of IL-17high CD4 TH cells (TH-17) and IL-17Rhigh B cells, and significantly increased numbers of type I interferon producing plasmacytoid dendritic cells in the spleens of these mice. We are currently studying the inter-connection of high IL-17, high type I IFN and the development of autoreactive B cells related to B-cell tolerance loss at the transitional stage and the germinal center stage in BXD2 mice.

    We currently study the close interaction between spleen marginal zone (MZ) B cells and MZ macrophages, and the implication of disrupting this close interaction in disease relapse following B-cell depletion therapy (BCDT) in systemic lupus erythematosus (SLE). In healthy individuals, the MZ B cells provide essential signals to maintain MZM survival and tolerogenic signaling to apoptotic debris derived autoantigens (AC-Ags) in the spleen MZ barrier. In SLE, a deficiency of tolerogenic MZMs occurs which disrupts the barrier and promotes an immunogenic environment including accumulation of uncleared AC-Ags and production of type I IFNs. Based on these results, we propose that BCDT in lupus, through depletion of the MZ B cells leads to a secondary depletion of the MZMs which may enable immunogenic responses to ACs in certain SLE patients. During deep B-cell depletion, when there are minimal B cells, this effect is not apparent. However, as B-cell repopulation occurs, the B cells are immediately subject to the immunogenic MZ microenvironment resulting in formation of autoreactive B cells and disease flares. We are currently developing strategies to overcome the loss of tolerogenic MZM barrier following BCDT with an ultimate goal to re-set B-cell tolerogenic state to achieve long-term remission. This work is currently supported by the Lupus Research Institute. http://lupusresearchinstitute.org/lupus-research/grant-recipients/hsu/hui-chen

     

    Publications

    Click here for a more complete list of publications on PubMed. Below are a few selected papers.


    Li H, Fu Y-X, Wu Q, Zhou Y, Crossman DK, Yang PA, Li J, Luo B, Morel LM, Kabarowski JH, Yagita H, Ware C, Hsu H-C, Mountz JD. 2015. Interferon-induced Defective Mechanosensing Signaling in Lupus Spleen Marginal Zone Macrophages. J Clin Invest. 125(7):2877-90. PMC4563689


    Hamilton JA, Li J, Wu Q, Yang PA, Luo B, Li H, Bradley JE, Taylor JE, Randall TD, Mountz JD, and Hsu H-C. 2015. General Approach for Tetramer Based Identification of Autoantigen Reactive B Cells: Characterization of La and snRNP Reactive B Cells in Autoimmune BXD2 Mice. J Immunol, 194(10):5022-34. PMC4417409


    Li H, Hsu H-C, Wu Q, Yang PA, Li J, Luo B, Cua D, Oukka M, Steele III CH, Grizzle, WE, and Mountz JD. 2014.  IL-23 promotes TCR-mediated negative selection of thymocytes through the upregulation of IL-23 receptor and RORγt. Nat Commun. 5:4259.  PMC4136447


    Li H, Wu Q, Li J, Yang P, Zhu Z, Luo B, Hsu H-C, and Mountz JD. 2013. Cutting Edge: Defective follicular exclusion of apoptotic antigens due to marginal zone macrophage defects in autoimmune BXD2 mice. J Immunol 190(9):4465-9. PMC3656168.


    Wang JH, New JS, Xie S, Yang PA, Wu Q, Li J, Luo B, Ding Y, Druey KM, Hsu H-C, and Mountz JD. 2013. Extension of the germinal center stage of B-cell development promotes autoantibodies in BXD2 mice. Arthritis & Rheum 65(10), 2703-2712. (Supplementary Table) PMC3979745

     

  • laura_hughesProfessor of Medicine
    Director, Rheumatology Fellowship Training Program

     

    Address:

    Shelby Bldg, Room 178G
    1825 University Blvd.
    35294-2182

    Telephone: (205) 934-7995
    Fax:(205) 996-6734
    Email:lhughes@uab.edu

     

    Education

    BS (Zoology), Auburn University, Auburn, Alabama, 1991, cum laude
    MD, University of Alabama at Birmingham, Birmingham, Alabama, 1996, with Scholastic Excellence
    Internship and Residency (Internal Medicine), Carraway Methodist Medical Center, Birmingham, Alabama, 1996-1999
    Chief Resident (Internal Medicine), Carraway Methodist Medical Center, Birmingham, Alabama, 1999-2000
    Clinical Fellow (Internal Medicine), Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama , 2001-2003
    MSPH (Clinical Trials/Biostatistics), University of Alabama at Birmingham, Birmingham, Alabama, 2001-2003

     

    Research Interests:

    Dr. Hughes’ research interest is in identifying pharmacogenetic markers for treatment response and toxicity in subjects with rheumatoid arthritis. She has also investigated genetic markers for susceptibility and severity in African-American subjects with rheumatoid arthritis. Her research interests have recently expanded to include analysis of genetic markers in inflammatory and adipokine genes for association with osteoarthritis.

     

    Publications

    Click here for a more complete list of publications. Below are a few selected papers.


    Tamhane A, McGwin G Jr, Redden DT, Hughes LB, Brown EE, Westfall AO, Reynolds RJ, Conn DL, Jonas BL, Smith EA, Brasington RD, Moreland LW, Bridges SL Jr, Callahan LF. 2013. Complementary and alternative medicine use in african-americans with rheumatoid arthritis. Arthritis Care Res (Hoboken). 66(2):180-189. PMID:23983105


    Reynolds RJ, Cui X, Vaughan LK, Redden DT, Causey Z, Perkins E, Shah T, Hughes LB; CLEAR Investigators, Damle A, Kern M, Gregersen PK, Johnson MR, Bridges SL Jr. 2013. Gene expression patterns in peripheral blood cells associated with radiographic severity in African Americans with early rheumatoid arthritis. Rheumatol Int. 33(1):129-37. PMID:22238028 PMCID:PMC3769702


    Perkins EA, Landis D, Causey ZL, Edberg Y, Reynolds RJ, Hughes LB, Gregersen PK, Kimberly RP, Edberg JC, Bridges SL Jr; Consortium for the Longitudinal Evaluation of African Americans with Early Rheumatoid Arthritis Investigators. 2012. Association of single-nucleotide polymorphisms in CCR6, TAGAP, and TNFAIP3 with rheumatoid arthritis in African Americans. Arthritis Rheum. 64(5):1355-8. PMID:22127930


    Guermazi A, Roemer FW, Hayashi D, Crema MD, Niu J, Zhang Y, Marra MD, Katur A, Lynch JA, El-Khoury GY, Baker K, Hughes LB, Nevitt MC, Felson DT. 2011. Extended report: assessment of synovitis with contrast-enhanced MRI using a whole-joint semiquantitative scoring system in people with, or at high risk of, knee osteoarthritis: the MOST study. Ann Rheum Dis. 70(5):805-11.  PMID: 21187293


    Hughes LB, Reynolds RJ, Brown EE, Kelley JM, Thomson B, Conn DL, Jonas BL, Westfall AO, Padilla MA, Callahan LF, Smith EA, Brasington RD, Edberg JC, Kimberly RP, Moreland LW, Plenge RM, Bridges SL Jr. 2010. Most common single-nucleotide polymorphisms associated with rheumatoid arthritis in persons of European ancestry confer risk of rheumatoid arthritis in African Americans. Arthritis Rheum. 62(12):3547-53. PMID: 21120996

     

     

  • RevTracy Hwangpo smallInstructor of Medicine

    Division of Clinical Immunology and Rheumatology

    Address:

    Shelby Building, Room 412
    1825 University Boulevard
    Birmingham, AL 35294-1711

    Telephone: (205) 934-7427

    Fax: (205) 934-1564

    Email: thwangpo@uabmc.edu


    Education:


    B.S.
    (Biology with Honors): Haverford College, 2000
    Ph.D.(Biomedical Sciences): Mount Sinai's Graduate School of Biomedical Sciences, 2007
    M.D.: Icahn School of Medicine at Mount Sinai, 2008
    Intern (Medicine): University of Alabama at Birmingham School of Medicine, Birmingham, AL, 2008-2009
    Resident (Medicine): University of Alabama at Birmingham School of Medicine, Birmingham, AL, 2009-2011
    Postdoctoral Fellow (Immunology): University of Alabama at Birmingham School of Medicine, Birmingham, AL, 2011-2014
    Clinical Fellow (Allergy & Immunology), University of Alabama at Birmingham School of Medicine, Birmingham, AL, 2012-2014

    Research Interests

     

    The focus of my research is the characterization of immune abnormalities in patients with recurrent sino-pulmonary infections with subnormal immunoglobulin levels, who do not meet criteria for Common Variable Immunodeficiency (CVID). As a clinician, I am interested in classifying those patients, as well as patients with classical CVID by severity and following the course of changes in their immune system to find clues that may suggest ways to treat their unspecified immunodeficiency. As a researcher, I have used several criteria to explore the immune abnormalities in this specific cohort: (a) Changes in B cell subsets as a function of time; (b) Functional antibody response; (c) HLA typing to examine the propensity for development of immunodeficiency; and (d) Examination of rare SNPs that may correlate with the severity of their immune system abnormalities.

     

    Publications


    Wang Y, Hwangpo T, Martin MP, Vince N, Qi Y, Reynolds RJ 4th, Absher D, Gao X, Ballinger CA, Burrows PD, Atkinson TP, Brown EE, Elgavish A, Liu C, Carrington M, Schroeder HW.J 2016. Killer cell immunoglobulin-like receptors are associated with common variable immune deficiency pathogenesis. Allergy Clin Immunol. 138:1495-1498. PMID: 27665490 PMCID: PMC5104182


    Mroczek, E, Ippolito, GC, Rogosch, T, Hoi, KH, Hwangpo, TA, Brand, MG Zhuang, Y, Liu,C, Schneider, D, Zemlin, M, Brown, EE, Georgiou, G, and Schroeder, HW. Differences in the composition of the human antibody repertoire by B cell subsets in the blood. Front. Immunol. 5:96, 2014. PMCID: PMC3958703


    Hwangpo, TA, Jordan, JD, Premsiriut,P, Jayamaran, G, Licht, J, Iyengar, R, and Neves, SR. GRIN modulates Sprouty repression of MAPK activation by growth factor stimulation. Journal of Biological Chemistry 287(17):13674-85. 2012. PMCID: PMC3340172

     

     

     

  • JainAssistant Professor of Medicine
    Division of Clinical Immunology & Rheumatology

    Address: 
     

    Faculty Office Tower, room 834
    510 20th Street South
    35294-2182

    Telephone:(205) 934-1532

     

    Education

    MD,Maulana Azad Medical College, Delhi University, New Delhi, India, 2001
    Internship(Internal Medicine), St. Francis Hospital, Evanston, IL, 2003-2004
    Residency (Internal Medicine), St. Francis Hospital, Evanston, IL, 2004-2005
    Chief Resident (Internal Medicine), St. Francis Hospital, Evanston, IL, 2005-2006

     

    Research and Clinical Interests

    Clinical interests include inflammatory arthritis, SLE, vasculitides, inflammatory myopathies, utilization of musculoskeletal ultrasound as a tool for evaluation of rheumatic disease. Main research interest is the safety of biological therapies in rheumatic diseases.

     

    Selected Publications

    Singh JA, Furst DE, Bharat A, Curtis JR, Kavanaugh AF, Kremer JM, Moreland LW, O'Dell J, Winthrop KL, Beukelman T, Bridges SL Jr, Chatham WW, Paulus HE, Suarez-Almazor M, Bombardier C, Dougados M, Khanna D, King CM, Leong AL, Matteson EL, Schousboe JT, Moynihan E, Kolba KS, Jain A, Volkmann ER, Agrawal H, Bae S, Mudano AS, Patkar NM, Saag KG. 2012. 2012 update of the 2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis. Arthritis Care Res (Hoboken). 64(5):625-39. PMCID: PMC4081542


    Singh JA, Furst DE, Bharat A, Curtis JR, Kavanaugh AF, Kremer JM, Moreland LW, O'Dell J, Winthrop KL, Beukelman T, Bridges SL Jr, Chatham WW, Paulus HE, Suarez-Almazor M, Bombardier C, Dougados M, Khanna D, King CM, Leong AL, Matteson EL, Schousboe JT, Moynihan E, Kolba KS, Jain, A, Volkman, ER, Agrawal, H, Bae, S, Mudano, AS, Patkar, NM, Saag, KG.2012 Update of the 2008 American College of Rheumatology (ACR) Recommendations for the use of Disease-Modifying Anti-Rheumatic Drugs (DMARDs) and Biologics in the treatment of Rheumatoid Arthritis (RA). Arthritis Care Res64(5):625-39. PMID: 22473917


    Curtis JR, Jain A, Askling J, Bridges SL Jr, Carmona L, Dixon W, Finckh A et al. 2010. A Comparison of Patient Characteristics and Outcomes in Selected European and U.S. Rheumatoid Arthritis Registries. Semin Arthritis Rheum.40(1):2-14.e1.PMID: 20674669


    Curtis JR, Patkar NM, Jain A, Greenberg J, Solomon DH. 2009. The Validity of Physician-Reported Hospitalized Infections in an Observational U.S. Arthritis Registry. Rheumatology (Oxford).48(10):1269-72. PMID: 19654217

     

     

  • kimberly CCTS croppedHoward L. HolleyProfessor of Medicine

    Director, UAB Center for Clinical and Translational Science


    Address: 

    Shelby Building, Room 172D
    1825 University Boulevard
    35294-2182

    Telephone:(205) 934-0245
    Email:rpk@uab.edu

     

    Program Manager I: Ms. Ronda Smith
    Shelby Building, Room 172D
    1825 University Blvd.
    Birmingham, AL35294-2182
    Telephone:205-934-0245
    Fax: 205-934-1564
    Email: rhsmith@uab.edu 
     

    Education


    AB,
    Princeton University
    BA, University of Oxford, Oxford, England
    MA (Physiology), University of Oxford, Oxford, England
    MD,Harvard Medical School
    Internship,University of Pennsylvania
    Residency, University of Pennsylvania Hospital
    Fellowship, Arthritis and Rheumatism Branch, NIAMS/NIH
    Fellowship, Hospital for Special Surgery, Cornell Medical Center
    Fellowship, Rheumatic Diseases, Hospital for Special Surgery, Cornell Medical Center


    Research Description

    Dr. Kimberly is an internationally recognized translational scientist with substantial experience in the development and administration of large, multi-site and multiple-investigator scientific programs.  His research group is interested in the role of genetic factors in the normal function of the immune system and in the development of autoimmune and immune-mediated inflammatory diseases such as systemic lupus erythematosus (SLE) and systemic vasculitis. The group’s approach has focused on receptors for immunoglobulin (Fc receptors) as a model system and has explored molecular mechanisms of receptor signaling and the molecular basis for receptor polymorphisms in humans. Allelic variations in receptor structure profoundly affect receptor function. The team has been a leader in developing several national and international research consortia for the study of human diseases, and they have demonstrated that certain low-binding alleles are enriched in SLE patients. More active alleles are over-represented in patients with vasculitis and severe renal disease. As prominent contributors in major population-based genome wide association studies, the group is pursuing other genes and gene families as they are identified as candidate genes. These genes include complement receptors, cytokine genes and their promoters, signal transduction molecules, and members of the TNF superfamily. In addition to identifying susceptibility alleles, these studies have led to molecular insights into responsiveness to Ig-based therapeutics.

     

    Publications

    Click here for a more complete list of publications. Below are a few selected papers.


    Kelley JM, Monach PA, Ji C, Zhou Y, Wu J, Tanaka S, Mahr AD, Johnson S, McAlear C, Cuthbertson D, Carette S, Davis JC Jr, Dellaripa PF, Hoffman GS, Khalidi N, Langford CA, Seo P, St Clair EW, Specks U, Stone JH, Spiera RF, Ytterberg SR, Merkel PA, Edberg JC, Kimberly RP. 2011. IgA and IgG antineutrophil cytoplasmic antibody engagement of Fc receptor genetic variants influences granulomatosis with polyangiitis. Proc Natl Acad Sci U S A. 108(51):20736-41. PMID:22147912


    Li X1, Wu J, Ptacek T, Redden DT, Brown EE, Alarcón GS, Ramsey-Goldman R, Petri MA, Reveille JD, Kaslow RA, Kimberly RP, Edberg JC. 2013. Allelic-dependent expression of an activating Fc receptor on B cells enhances humoral immune responses. Sci Transl Med. 5(216):216ra175. PMCID:PMC3982386


    Freedman BI1, Langefeld CD, Andringa KK, Croker JA, Williams AH, Garner NE, Birmingham DJ, Hebert LA, Hicks PJ, Segal MS, Edberg JC, Brown EE, Alarcón GS, Costenbader KH, Comeau ME, Criswell LA, Harley JB, James JA, Kamen DL, Lim SS, Merrill JT, Sivils KL, Niewold TB, Patel NM, Petri M, Ramsey-Goldman R, Reveille JD, Salmon JE, Tsao BP, Gibson KL, Byers JR, Vinnikova AK, Lea JP, Julian BA, Kimberly RP; Lupus Nephritis–End‐Stage Renal Disease Consortium. 2014. End-stage renal disease in African Americans with lupus nephritis is associated with APOL1. Arthritis Rheumatol. 66(2):390-6. PMCID:PMC4002759

     

     

     

  • JunLi Updated 2013Instructor of Medicine

    Division of Clinical Immunology and Rheumatology

    Address:

    Shelby Building, Suite 337
    1825 University Boulevard
    Birmingham, AL 35294-2182

    Telephone: (205) 934-8909

    Fax: (205) 996-6788

    Email: junli@uabmc.edu

     

    Education:

    M.D.Sun Yat-sen University, School of Medicine, Guangzhou, China 1997
    Ph.D.(Physiology): University of Alabama at Birmingham, 2008
    Postdoctoral Fellow: Department of Medicine, Division of Clinical Immunology & Rheumatology, University of Alabama at Birmingham, 2012

     

    Research Interests

    Macrophages in pathogenesis of rheumatoid arthritis (RA) and development of novel macrophage target therapies in RA; Identification of novel markers (death receptor, et al) of M1 inflammatory macrophages in RA;


    figure-1

    Roles of fucosylation in regulation of macrophage differentiation, apoptosis, antigen presentation, cytoskeleton rearrangement, and how these are linked to pathogenesis of RA; efficacy and mechanisms of fucosylation inhibitors in the treatment of RA and other autoimmune diseases;

    figure-2-2

    Studies of inflammatory IRF5+ macrophages and GM-CSF+ CD4 T cell interaction in RA using synovial fluid and PBMC from RA subjects. 


    Figure-3-2

     

    Publications

    Click here for a more complete list of publications. Below are selected papers


    Li J,
    Hsu HC, Ding Y, Li H, Wu Q, Yang P, Luo B, Rowse AL, Spalding DM, Bridges SL Jr, Mountz JD. 2014. Inhibition of fucosylation reshapes inflammatory macrophages and suppresses type II collagen-induced arthritis. Arthritis Rheumatol. 66(9):2368-79. PMC4146698


    Li J, Yang PA, Wu Q, Li, H, Ding Y, Hsu H-C, Spalding DM, and Mountz JD. 2013. Death receptor 5-targeted depletion of interleukin 23 producing macrophages, Th17, and Th1/17 associated with defective tyrosine phosphatase in mice and patients with rheumatoid arthritis. Arthritis & Rheum 65(10), 2594-2605. (Supplementary Table). PMC3993980


    Li J
    , Hsu H-C, and Mountz JD.  2012. Managing Macrophage in Rheumatoid Arthritis by Reform or Removal. Curr Rheumatol Rep. 14 (5):445-54. PMID: 22855296


    Li J
    , Hsu H-C, Yang P, Wu Q, Li H,  Edgington LE, Bogyo M, Kimberly RP, and Mountz JD.  2012. Treatment of Arthritis by Macrophage Depletion and Immunomodulation: Testing an Apoptosis-Mediated Therapy in a Humanized Death Receptor Mouse Model. Arthritis Rheum. 64(4):1098-109.  PMID: 22006294

     

  • Assistant Professor of MedicineXiaoli-Li

    Address:
     

    Shelby Bldg, Room 205
    1825 University Blvd
    35294-2182

    Telephone:(205) 996-4477
    Fax:(205) 975-4404
    Email:xili@uabmc.edu
     

    Education


    Diploma,Wuhan University, China, 1979
    MS,Wuhan University, China, 1982
    PhD,University of Alabama at Birmingham, 1992
    Post-Doctoral Training (Immunology):Cleveland Clinic Foundation, 1992-1994

    Post-Doctoral Training:University of Alabama at Birmingham, 1995-1997

    Research Description

     
    Dr. Li's major research interest is investigation of biological effects of Fcγ Receptor polymorphisms. Elucidation of the biological functions mediated by Fcγ Receptors.
     

    Publications

    Click here for a more complete list of publications. Below are a few selected papers.


    Li X, Baskin JG, Mangan EK, Su K, Gibson AW, Ji C, Edberg JC, Kimberly RP. 2012. The unique cytoplasmic domain of human FcγRIIIA regulates receptor-mediated function. J Immunol. 189(9):4284-94.  PMC3478424 PMID:23024279 


    Su K, Yang H, Li X, Li X, Gibson AW, Cafardi JM, Zhou T, Edberg JC, Kimberly RP. 2007. Expression profile of FcgammaRIIb on leukocytes and its dysregulation in systemic lupus erythematosus. J Immunol. 178(5):3272-80. PMID: 17312177

     
    Su K, Li X, Edberg JC, Wu J, Ferguson P, Kimberly RP. 2004. A promoter haplotype of the immunoreceptor tyrosine-based inhibitory motif-bearing FcgammaRIIb alters receptor expression and associates with autoimmunity. II. Differential binding of GATA4 and Yin-Yang1 transcription factors and correlated receptor expression and function. J Immunol. 172(11):7192-9. PMID: 15153544

     
    Su K, Wu J, Edberg JC, Li X, Ferguson P, Cooper GS, Langefeld CD, Kimberly RP. 2004. A promoter haplotype of the immunoreceptor tyrosine-based inhibitory motif-bearing FcgammaRIIb alters receptor expression and associates with autoimmunity. I. Regulatory FCGR2B polymorphisms and their association with systemic lupus erythematosus. J Immunol. 172(11):7186-91.

     

  • Sarah-MorganProfessor of Medicine
    Medical Director, Osteoporosis Clinic, Center for Metabolic Bone Disease


    Address:

    830 Faculty Office Tower
    510 20th Street South
    Birmingham, AL 35294-3408

    Telephone:(205) 934-3235
    Fax:(205) 934-4602
    Email:slmorgan@uab.edu

     

    Education

    BS (Nutrition and Dietetics), Iowa State University, 1977
    BS (Nutrition and Related Sciences), Iowa State University, 1977
    MD, The University of Iowa, 1981
    Internship and Residence (Internal Medicine), University of Iowa Hospitals and Clinics, Iowa City, 1981-1984
    Fellowship (Clinical Nutrition), The University of Alabama at Birmingham, 1984-1986
    MS (Nutrition), The University of Alabama at Birmingham, 1987

     

    Honors:

    C.E. Butterworth Award, UAB - 1986
    Outstanding Young Alumna, Iowa State University, 1991
    Outstanding Young Alumna, UAB Department of Nutrition Sciences, School of Health Related Professions
    Distinguished Achievement Citation, Iowa State University, 1999
    Outstanding UAB Woman Faculty Member, 2001
    Distinguished Alumlnus Award for Achievement, University of Iowa 2007
    UAB School of Health Professions - Member of "Fab 40" - 2009
    Sam Brown Bridge Builder Award, UAB, 2010
    President, International Society for Clinical Densitometry, 2011-2012

     

    Research Description

    Dr. Morgan's research program has been focused on methotrexate and folic acid metabolism in patients with rheumatoid arthritis.  Her work with Dr. Joseph E Baggott and members of the Division of Clinical Immunology and Rheumatology (Drs. Graciela Alarcon, Dr. William Koopman, Dr. S Louis Bridges, and Dr. Laura Hughes) have established the folic acid supplementation during low dose methotrexate therapy for rheumatoid arthritis lowers toxicity without affecting efficacy.  Drs Morgan and Baggott have also studied purine metabolism and methotrexate therapy in rat adjuvant arthritis and participate in trials related to methotrexate pharmacogenetics.  Dr. Morgan and Dr. Baggott have also investigated the effects of a medical food on osteoarthritis.

    As the Medical Director of the UAB Osteoporosis Prevention and Treatment Clinic, Dr. Morgan has an interest in bone densitometry and clinical trials related to osteoporosis.

     

    Publications

    Click here for a more complete list of publications. Below are selected papers.


    Morgan SL, Prater GL. 2017 Quality in dual-energy X-ray absorptiometry scans. Bone. 2017 Jan 31. [Epub ahead of print] PMID: 28159711


    Lewiecki EM, Binkley N, Morgan SL, Shuhart CR, Camargos BM, Carey JJ, Gordon CM, Jankowski LG, Lee JK, Leslie WD. 2016. Best practices for dual-energy x-ray absorptiometry measurement and reporting: International Society for Clinical Densitometry Guidance. J Clin Densitom 10: 127-40. PMID: 27020004


    Baggott JE, Bridges SL, Morgan SL.  2005. Evidence for two phenotypes in the metabolism of methotrexate to 7-hydroxymethotrexate in patients with rheumatoid arthritis.  Arthritis Rheum 52: 356-358. PMID: 15641087


    Morgan SL, Baggott JE, Vaughn WH, Austin JS, Veitch TA, Lee JY, Koopman WJ, Krumdieck CL, Alarcón GS. 1994. Supplementation with folic acid during methotrexate therapy of rheumatoid arthritis: results from a double-blind, placebo-controlled trial.  Ann Intern Med 121: 833-841. PMID:7978695


    Morgan SL, Baggott JE, Vaughn WH, Young PK, Austin JV, Krumdieck CL, Alarcón GS.  1990. The effect of folic acid supplementation on the toxicity of low-dose methotrexate treatment of rheumatoid arthritis.  Arthritis Rheum 33:  9-18. PMID: 2405864

     

     

     

SOM Epilogue Menu