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

Semin Immunol. 2007 Feb;19(1):11-23. doi: 10.1016/j.smim.2006.12.005. Epub 2007 Feb 2.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Autoantibodies / biosynthesis*
  • B-Lymphocytes / immunology*
  • Humans
  • Lupus Erythematosus, Systemic / immunology
  • Lupus Erythematosus, Systemic / physiopathology*
  • Lymphocyte Activation
  • Toll-Like Receptors / immunology
  • Toll-Like Receptors / metabolism*


  • Autoantibodies
  • Toll-Like Receptors