Toll-like Receptors Control Activation of Adaptive Immune Responses

Nat Immunol. 2001 Oct;2(10):947-50. doi: 10.1038/ni712.

Abstract

Mechanisms that control the activation of antigen-specific immune responses in vivo are poorly understood. It has been suggested that the initiation of adaptive immune responses is controlled by innate immune recognition. Mammalian Toll-like receptors play an essential role in innate immunity by recognizing conserved pathogen-associated molecular patterns and initiating the activation of NF-kappaB and other signaling pathways through the adapter protein, MyD88. Here we show that MyD88-deficient mice have a profound defect in the activation of antigen-specific T helper type 1 (TH1) but not TH2 immune responses. These results suggest that distinct pathways of the innate immune system control activation of the two effector arms of adaptive immunity.

Publication types

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

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Animals
  • Antigens, Differentiation / genetics*
  • Caspase 1 / genetics
  • Cell Differentiation
  • Cells, Cultured
  • Dendritic Cells / immunology
  • Drosophila Proteins*
  • Immunoglobulins / biosynthesis
  • Interferon-gamma / biosynthesis
  • Interleukin-13 / biosynthesis
  • Lymphocyte Activation*
  • Membrane Glycoproteins / physiology*
  • Mice
  • Mice, Knockout
  • Myeloid Differentiation Factor 88
  • Phenotype
  • Receptors, Cell Surface / physiology*
  • Receptors, Immunologic*
  • Th1 Cells / immunology*
  • Th2 Cells / immunology
  • Toll-Like Receptors

Substances

  • Adaptor Proteins, Signal Transducing
  • Antigens, Differentiation
  • Drosophila Proteins
  • Immunoglobulins
  • Interleukin-13
  • Membrane Glycoproteins
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Toll-Like Receptors
  • Interferon-gamma
  • Caspase 1