Robert P. Kimberly, MDHoward L. Holley Professor

Director, UAB Center for Clinical and Translational Science


Shelby Building, Room 172D
1825 University Boulevard

Telephone:(205) 934-0245


Program Manager I: Ms. Ronda Smith
Shelby Building, Room 172D
1825 University Blvd.
Birmingham, AL35294-2182
Fax: 205-934-1564


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.



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




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