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Lupus
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Molecular mimicry in systemic lupus erythematosus

N. Agmon-Levin

Department of Medicine 'B', and The Center for Autoimmune Diseases Sheba Medical Center, Tel-Hashomer, Israel, Sackler Faculty of Medicine, Tel-Aviv University, Israel

M. Blank

Department of Medicine 'B', and The Center for Autoimmune Diseases Sheba Medical Center, Tel-Hashomer, Israel, Sackler Faculty of Medicine, Tel-Aviv University, Israel

Z. Paz

Department of Medicine 'B', and The Center for Autoimmune Diseases Sheba Medical Center, Tel-Hashomer, Israel, Sackler Faculty of Medicine, Tel-Aviv University, Israel

Y. Shoenfeld

Department of Medicine 'B', and The Center for Autoimmune Diseases Sheba Medical Center, Tel-Hashomer, Israel, Sackler Faculty of Medicine, Tel-Aviv University, Israel, Incumbent of the Laura Schwarz-Kip Chair for Research of Autoimmune Diseases, Tel-Aviv University, Israel, shoenfel{at}post.tau.ac.il

Systemic lupus erythematosus is a multi-systemic autoimmune disease distinguished by the presence of various autoantibodies. Like most autoimmune diseases, systemic lupus erythematosus is believed to be induced by a combination of genetic, immunologic, and environmental factors, mainly infectious agents. Molecular mimicry between an infectious antigen and self-components is implicated as a pivotal mechanism by which autoimmune diseases such as systemic lupus erythematosus are triggered. Here we review the current evidence of molecular mimicry between different infectious agents and systemic lupus erythematosus.

Key Words: autoantibodies • autoimmunity • cross-reactivity • Epstein—Barr virus • infections • molecular mimicry • systemic lupus erythematosus

Lupus, Vol. 18, No. 13, 1181-1185 (2009)
DOI: 10.1177/0961203309346653


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