The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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Published 19 July 2004. doi:10.1084/jem.20040526
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 2, 261-266
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Brief Definitive Report

 SH2D1A Regulates T-dependent Humoral Autoimmunity

Jonathan D. Hron1, Liron Caplan1, Andrea J. Gerth1, Pamela L. Schwartzberg3, and Stanford L. Peng1,2

1 Department of Internal Medicine/Rheumatology and 2 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110
3 National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892

Address correspondence to Stanford L. Peng, Washington University School of Medicine, Campus Box 8045, CSRB 6617, 660 S. Euclid Ave., St. Louis, MO 63110. Phone: (314) 747-3609; Fax: (314) 454-1091; email: speng{at}im.wustl.edu

The signaling lymphocytic activation molecule (SLAM)/CD150 family includes a family of chromosome 1–encoded cell surface molecules with costimulatory functions mediated in part by the adaptor protein SH2D1A (SLAM-associated protein, SAP). Deficiency in SH2D1A protects mice from an experimental model of lupus, including the development of hypergammaglobulinemia, autoantibodies including anti–double stranded DNA, and renal disease. This protection did not reflect grossly defective T or B cell function per se because SH2D1A-deficient mice were susceptible to experimental autoimmune encephalomyelitis, a T cell–dependent disease, and they were capable of mounting normal T-independent antigen-specific immunoglobulin responses. Instead, T-dependent antibody responses were impaired in SH2D1A-deficient mice, reflecting defective germinal center formation. These findings demonstrate a specific role for the SLAM–SH2D1A system in the regulation of T-dependent humoral immune responses, implicating members of the CD150–SH2D1A family as targets in the pathogenesis and therapy of antibody-mediated autoimmune and allergic diseases.

Key Words: autoimmunity • mice • knockout • lupus • T lymphocytes

J.D. Hron and L. Caplan contributed equally to this work.


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