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

 

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