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Toll-like receptor 2 ligands on the staphylococcal cell wall downregulate superantigen-induced T cell activation and

Thu A Chau1, Michelle L McCully, William Brintnell

  • 1FOCIS Centre for Clinical Immunology and Immunotherapeutics, Robarts Research Institute, London, Ontario, Canada.

Nature Medicine
|May 26, 2009
PubMed

Insights

Staphylococcus bacteria can suppress the immune system's T cell response to superantigens, preventing toxic shock syndrome. This bacterial immune evasion strategy involves peptidoglycan molecules that induce immune-suppressing interleukin-10.

Area of Science:

  • Immunology
  • Microbiology
  • Toxicology

Background:

  • Staphylococcal superantigens trigger potent T cell activation, leading to toxic shock syndrome.
  • Despite severe immune responses, staphylococcal infections are clinically prevalent, suggesting immune evasion mechanisms.

Purpose of the Study:

  • To investigate if staphylococcal strains downregulate T cell responses to superantigens.
  • To elucidate the mechanisms behind bacterial immune evasion during staphylococcal infections.

Main Methods:

  • Assessed the effect of simultaneous bacterial presence on interleukin-2 response to staphylococcal superantigens.
  • Investigated the role of peptidoglycan and Toll-like receptor 2 (TLR2) signaling.
  • Evaluated mortality in mouse models of toxic shock syndrome upon co-administration of superantigens and bacterial components.

Main Results:

  • Simultaneous bacterial presence significantly inhibited the interleukin-2 response to staphylococcal superantigens.
  • Peptidoglycan-embedded molecules binding to TLR2 induced interleukin-10 production and antigen-presenting cell apoptosis.
  • Heat-killed staphylococci or Staphylococcus aureus peptidoglycan administration prevented mortality in mouse models of toxic shock syndrome.

Conclusions:

  • Staphylococcal peptidoglycan actively downregulates T cell responses to superantigens via TLR2-mediated pathways.
  • This bacterial immune evasion strategy contributes to the common occurrence of staphylococcal infections despite potent superantigenicity.
  • Targeting these bacterial evasion mechanisms could offer new therapeutic strategies against staphylococcal diseases.

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