TLR-dependent T cell activation in autoimmunity

Nat Rev Immunol. 2011 Nov 18;11(12):807-22. doi: 10.1038/nri3095.


Autoimmune disease can develop as a result of a breakdown in immunological tolerance, leading to the activation of self-reactive T cells. There is an established link between infection and human autoimmune diseases. Furthermore, experimental autoimmune diseases can be induced by autoantigens that are administered together with complete Freund's adjuvant, which contains killed Mycobacterium tuberculosis; in some cases, these bacteria can be replaced by individual pathogen-associated molecular patterns (PAMPs). Exogenous PAMPs and endogenous danger signals from necrotic cells bind to pattern recognition receptors (including Toll-like receptors) and activate signalling pathways in innate immune cells and in T cells. This leads to pro-inflammatory cytokine production and T cell activation, which are now considered to be major factors in the development of autoimmunity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / physiology
  • Animals
  • Autoantigens / immunology
  • Autoimmunity / immunology*
  • Cell Death / immunology
  • Cytokines / physiology
  • Host-Pathogen Interactions / immunology
  • Humans
  • Infections / immunology
  • Inflammation / etiology
  • Inflammation / immunology
  • Intestines / immunology
  • Intestines / microbiology
  • Lymphocyte Activation / immunology*
  • Mice
  • Molecular Mimicry
  • Organ Specificity
  • Self Tolerance / immunology
  • T-Cell Antigen Receptor Specificity
  • T-Lymphocyte Subsets / immunology*
  • Th1 Cells / immunology
  • Th17 Cells / immunology
  • Toll-Like Receptors / immunology*


  • Adaptor Proteins, Signal Transducing
  • Autoantigens
  • Cytokines
  • Toll-Like Receptors