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Semin Immunol. 2007 Feb;19(1):11-23. Epub 2007 Feb 2.

Regulation of lupus-related autoantibody production and clinical disease by Toll-like receptors.

Author information

1
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520-8035, United States. sean.christensen@yale.edu

Abstract

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.

PMID:
17276080
PMCID:
PMC2709770
DOI:
10.1016/j.smim.2006.12.005
[Indexed for MEDLINE]
Free PMC Article

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