Journal
SEMINARS IN IMMUNOLOGY
Volume 19, Issue 1, Pages 11-23Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2006.12.005
Keywords
systemic lupus erythematosus; autoantibodies; Toll-like receptor-7; Toll-like receptor-9; anti-Sm; anti-chromatin; B cell; autoimmune disease
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Funding
- NIAID NIH HHS [R01 AI061090-01, P01 AI036529-060007, P01 AI036529, R01 AI052401-01, P01 AI036529-050007, P01-AI36529] Funding Source: Medline
- NIAMS NIH HHS [P01 AR050256-050003, R01 AR044077-07, P01-AR050256, P01 AR050256, R01 AR044077, R01 AR044077-08] Funding Source: Medline
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Autoantigens that contain DNA, RNA, or self-IgG are preferred targets for autoantibodies in systemic lupus erythematosus (SLE). B cells promote SLE pathogenesis by producing autoantibodies, activating autoreactive T cells, and secreting cytokines. We discuss how certain autoreactive B cells are selectively activated, with emphasis on the roles of key Toll-like receptors (TLRs). Although TLR7, which recognizes ssRNA, promotes autoimmune disease, TLR9, which recognizes DNA, unexpectedly regulates disease, despite being required for the secretion of anti-chromatin autoantibodies. We describe positive feedback loops involving B cells, T cells, DCs, and soluble mediators, and how these networks are regulated by TLR signals. (c) 2007 Elsevier Ltd. All rights reserved.
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