The contribution of direct TLR signaling to T cell responses

Immunol Res. 2009;45(1):25-36. doi: 10.1007/s12026-009-8113-x.

Abstract

It is well established that Toll-like receptors (TLRs) play a critical role in the generation of innate immune responses and thereby also play an important, indirect role in the initiation of subsequent adaptive T cell responses. However, T cells also express certain TLRs, and we have focused on the physiological importance of direct TLR signaling in T cells. TLRs can function as co-stimulatory receptors that complement TCR-induced signals to enhance effector T cell proliferation, survival and cytokine production. We also found that TLR signaling pathways in T cells are required for the effective clonal expansion of antigen-specific T cells during infection in vivo. Thus, the importance of TLRs in T cell-mediated immunity reflects both T cell-extrinsic and T cell-intrinsic components, which warrants a reconsideration of the dogma that restricts germ-line encoded pattern recognition to cells of the innate immune system.

MeSH terms

  • Animals
  • Antigens, CD / biosynthesis
  • Cell Proliferation
  • Cells, Cultured
  • Immunity, Innate
  • Interferon-gamma / biosynthesis*
  • Interferon-gamma / genetics
  • Interferon-gamma / metabolism
  • Interleukin-2 / biosynthesis*
  • Interleukin-2 / genetics
  • Interleukin-2 / metabolism
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myeloid Differentiation Factor 88 / genetics
  • Myeloid Differentiation Factor 88 / metabolism
  • Protein Binding
  • Receptors, Antigen, T-Cell / immunology*
  • Receptors, Antigen, T-Cell / metabolism
  • Signal Transduction / immunology*
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • T-Lymphocytes / pathology
  • Toll-Like Receptors / immunology*
  • Toll-Like Receptors / metabolism

Substances

  • Antigens, CD
  • Interleukin-2
  • Myeloid Differentiation Factor 88
  • Receptors, Antigen, T-Cell
  • Toll-Like Receptors
  • Interferon-gamma