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Keith Elkon, M.D.
Keith B. Elkon, M.D.
Professor, Medicine and Head, Division of Rheumatology
Dr. Elkon received his medical degree from the University of Witwatersrand, Johannesburg South Africa in 1974 and membership to the Royal College of Physicians (MRCP) in 1978. He received postdoctoral training at the Hammersmith Hospital, London and at the Weill Medical College of Cornell University, New York. Dr. Elkon was formerly Director of the Graduate Program in Immunology and Professor of Medicine at Cornell. He was appointed as Head, Division of Rheumatology, at UW in August, 2001.
Department of Medicine
University of Washington
Office BB-561, HSC, Box 356428
1959 NE Pacific Street
Seattle WA 98195
Dr. Elkon's research objective is to better define the molecular and genetic basis for autoimmune diseases such as lupus and arthritis. Current areas of investigation include the following:
Apoptosis and the Immune Response – especially as it relates to lupus (SLE). Loss of tolerance leads to autoantibody production in systemic autoimmune disorders such as systemic lupus erythematosus (SLE). There is considerable evidence to support the concept that autoantibodies are generated in response to impaired clearance of dead and dying cells. Dr. Elkon's laboratory has identified novel pathways that involve opsonization of dying cells by serum factors (complement, CRP and natural antibodies) thereby promoting the phagocytosis of apoptotic cells. Deficiencies of these serum opsonins leads to delayed clearance of dying cells sequentially facilitating necrosis, an inflammatory response to self antigens and loss of tolerance. Current studies explore the how self antigens (e.g. nucleoprotein particles such as nucleosomes, spliceosomes and ribosomes) are processed and activate the innate immune system, especially plasmacytoid dendritic cells (pDCs) to induce IFN-a. In addition, apoptotic cell processing and the downstream molecular signals in DCs that lead to anergy or T cell activation are being investigated.
Removal of inflammatory nucleoprotein complexes. A related line of investigation explores how the debris derived from apoptotic cells, nucleoprotein particles, can be rendered less immunogenic. The research involves the creation of transgenic mice expressing "cleanup" molecules as well as biologics that can be administered exogenously.
1. Giltiay NV, Chappell CP, Sun X, Kolhatkar N, Teal T, Wiedeman A, Kim J, Tanaka L, Buechler MB, Hamerman JA, Imanishi-Kari T, Clark EA, Elkon KB. Overexpression of TLR7 promotes cell-intrinsic expansion and autoantibody production by transitional T1 B cells. J Exp Med, Oct 21, 2013 [Epub ahead of print].
2. Wiedeman A, Santer DM, Yan W, Miescher S, Kaisermann F, Elkon KB. Contrasting mechanisms of interferon‐α inhibition by intravenous immunoglobulin after stimulation with immune complexes versus toll like receptor agonists. Arthritis Rheum, 65:2713-23 2013.
3. Sun XZ, Wiedeman A, Agrawal N, Teal TH, Tanaka L, Hudkins KL, Alpers CE, Bolland S, Buechler M, Hamerman JA, Ledbetter JA, Liggitt D, Elkon KB. Increased RNase expression reduces inflammation and prolongs survival in TLR7 transgenic mice. J Immunol, 190:2536-2543, 2013.
4. Santer DM, Wiedeman AE, Teal T, Ghosh P, Elkon KB. Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes. J Immunol, 188:902-15, 2012.
5. Peng Y, Elkon KB. Autoimmunity in MFG-E8-deficient mice is associated with altered trafficking and enhanced cross-presentation of apoptotic cell antigens. J Clin Invest. 121:2221-41, 2011.
6. Briggs TA, Rice GI, Daly S, Urquhart J, Gornall H, Bader-Meunier B, Baskar K, Baskar S, Baudouin V, Beresford MW, Black GC, Dearman RJ, de Zegher F, Foster ES, Francès C, Hayman AR, Hilton E, Job-Deslandre C, Kulkarni ML, Le Merrer M, Linglart A, Lovell SC, Maurer K, Musset L, Navarro V, Picard C, Puel A, Rieux-Laucat F, Roifman CM, Scholl-Bürgi S, Smith N, Szynkiewicz M, Wiedeman A, Wouters C, Zeef LA, Casanova JL, Elkon KB, Janckila A, Lebon P, Crow YJ. Tartrate-resistant acid phosphatase deficiency causes a bone dysplasia with autoimmunity and a type I interferon expression signature. Nat Genet. 43:127-31, 2011.
7. Santer DM, Hall BE, George TC, Tangsombatvisit S, Liu CL, Arkwright PD, Elkon KB.C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes. J Immunol. 185:4738-49, 2010
8. Elkon, KB, Ronnblom L. Cytokines as therapeutic targets in SLE. Nat Rev Rheumatol, 6:339-347, 2010.
M.D., University of Witwatersrand
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