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Mary Kirkland Center for Lupus Research

2008-2011 Kirkland Scholar

Keith B. Elkon, MD

Professor of Medicine and Adjunct Professor of Immunology
University of Washington (UW), Seattle

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 where he worked for 20 years. 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.

Dr. Elkon's research objective is to better define the molecular and genetic basis for systemic autoimmune diseases such as lupus (SLE). He has made a number of contributions to the identification of autoantibody specificities in SLE and was the first to link cytoplasmic reactivity of lupus sera to the ribosomal P proteins. His laboratory mapped the P protein epitopes, developed an immunoassay and showed that anti-P antibodies were associated with neuropsychiatric lupus (NPSLE). Since 1994, Dr Elkon's laboratory has focused on pathways of apoptosis and processing of apoptotic cells showing how defects in these pathways lead to immune responses to self. He examined Fas (CD95) expression in SLE and identified molecular and genetic defects in the Fas pathway in children with Canale-Smith syndrome (also known as ALPS). Most recently, he has identified physiologic pathways of clearance of apoptotic cells and examined how manipulation of these pathways influence autoimmunity in experimental animals. Current studies focus on how aberrant handling of dying cells lead to inflammation and type 1 interferon in particular in both murine and human autoimmunity.

Representative recent publications:

  • Gershov D, Kim S-J, Brot N, Elkon KB. C-reactive protein binds to apoptotic cells, protects the cells from assembly of the terminal complement components and sustains an anti-inflammatory innate immune response: implications for systemic autoimmunity, J Exp Med, 192: 1353-1363, 2000.
  • Kim S-J, Gershov D, Brot N, Elkon KB. I-PLA2 activation during apoptosis promotes the exposure of membrane lysophosphatidylcholine leading to binding by natural IgM antibodies and complement activation. J Exp Med, 196: 655-665, 2002.
  • Kim SJ, Elkon KB, Ma X. Transcriptional suppression of interleukin-12 gene expression following phagocytosis of apoptotic cells. Immunity 2004;21:643-53.
  • Martin, D.A., and K.B. Elkon. 2005. Autoantibodies make a U-turn: the toll hypothesis for autoantibody specificity. J Exp Med 202:1465-1469, 2005.
  • Martin, D.A., Elkon, KB. Intracellular mammalian DNA stimulates myeloid dendritic cells to produce Type I interferons independently of MyD88 or TLR9. Arthritis Rheum, 54:951-962., 2006.
  • Martin DM, Zhang K, Kenkel J, Hughes G, Clark E, Davidson A, Elkon KB. Autoimmunity stimulated by adoptively transferred dendritic cells is initiated by both a/b and g/d T-cells but does not require MyD88 signaling. J Immunol, 179: 5819-5828, 2007.
  • Okamoto A, Fujio K, van Rooijen N, Tsuno NH, Takahashi K, Tsurui H, Hirose S, Elkon KB, Yamamoto K. Splenic phagocytes promote responses to nucleosomes in (NZB x NZW) F1 mice. J Immunol, 181:5264-5271, 2008.
  • Santer DM, Yoshio T, Minota S, Möeller T, Elkon KB. Potent induction of interferon-a and chemokines by autoantibodies in the cerebrospinal fluid of patients with neuropsychiatric lupus. J Immunol, 182:1192-1201. 2009.
  • Peng YF, Latchman Y, Elkon KB. Monocytes differentiate into dendritic cells and cross-tolerize T cells through PDL-1, J Immunol, 182: 2777-2785, 2009.