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T cell receptor V gene usage by human T cells stimulated with the superantigen streptococcal M protein

M A Tomai1, J A Aelion, M E Dockter

  • 1Veteran's Administration Medical Center, Memphis, Tennessee 38104.

The Journal of Experimental Medicine
|July 1, 1991
PubMed

Insights

Group A streptococci M proteins act as superantigens, stimulating T cells. This study shows M protein selectively activates T cells expressing specific T cell receptor V beta chains, potentially causing autoimmune diseases.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • M proteins are key virulence factors of Group A Streptococcus (GAS).
  • GAS M proteins are implicated in acute rheumatic fever (ARF) and related autoimmune conditions.
  • A specific M protein fragment (22-kD of M type 5) functions as a superantigen.

Purpose of the Study:

  • To investigate the T cell receptor (TCR) usage in response to a streptococcal M protein superantigen.
  • To determine if M protein superantigen exhibits specific T cell receptor V alpha element usage.
  • To elucidate the role of TCR usage in M protein-mediated pathogenesis of post-streptococcal diseases.

Main Methods:

  • Flow cytometry was used to analyze T cell populations.
  • Polymerase chain reaction (PCR) was employed to assess T cell receptor gene expression.
  • TCR V beta and V alpha usage was analyzed in T cells stimulated with M protein fragment (pep M5).

Main Results:

  • The M protein fragment specifically stimulated T cells expressing TCR V beta 2, 4, and 8 elements.
  • Preferential usage of specific TCR V alpha elements was observed but was individual-dependent, not superantigen-specific.
  • A large expansion of T cells with specific TCR V beta sequences was induced by the M protein.

Conclusions:

  • M protein-induced expansion of T cells with specific TCR V beta chains contributes to the pathogenesis of post-streptococcal autoimmune diseases.
  • Individual variations in TCR V alpha usage may influence susceptibility to developing self-reactivity after streptococcal infections.

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