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Identification of streptococcal m-protein cardiopathogenic epitopes in experimental autoimmune valvulitis

Christine A Kirvan1, Jeffrey E Galvin, Silvia Hilt

  • 1Department of Biological Sciences, California State University, Sacramento, CA, USA.

Journal of Cardiovascular Translational Research
|December 19, 2013
PubMed

Insights

Rheumatogenic group A streptococci M protein causes heart valve inflammation. Specific M5 protein T cells, particularly those recognizing peptide NT5/6, are key mediators in this valvulitis model.

Area of Science:

  • Immunology
  • Microbiology
  • Cardiovascular Research

Background:

  • Rheumatogenic group A streptococci M protein is implicated in rheumatic heart disease pathogenesis.
  • M protein induces carditis and valvulitis in Lewis rats, suggesting a role in disease development.

Purpose of the Study:

  • To identify specific epitopes within the M5 protein that elicit valvulitis.
  • To elucidate the role of T cells in M protein-induced valvulitis.

Main Methods:

  • Synthetic peptides representing M5 protein repeat regions were synthesized and tested for valvulitis induction.
  • T cell lines from affected rats were generated and characterized.
  • Passive transfer experiments using T cell lines were performed in naive rats.

Main Results:

  • M5 protein peptides NT4, NT5/6, and NT7 induced valvulitis.
  • T cell lines from valvulitis-affected rats recognized M5 peptides NT5/6 and NT6.
  • Passive transfer of an NT5/6-specific T cell line induced valvulitis with CD4+ cell infiltration and VCAM-1 upregulation.

Conclusions:

  • M protein-specific T cells, particularly those recognizing the NT5/6 epitope, are critical mediators of valvulitis.
  • These findings highlight the role of T cell-mediated immunity in the Lewis rat model of rheumatic carditis.

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