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Related Experiment Videos

Rheumatic fever: how S. pyogenes-primed peripheral T cells trigger heart valve lesions.

L Guilherme1, K C Faé, S E Oshiro

  • 1Laboratório de Imunologia, Instituto do Coração (HC-FMUSP), School of Medicine, University of São Paulo, Av. Dr. Eneas de Carvalho Aguiar, 44-9 andar., 05403-000 São Paulo, SP, Brazil. luizagui@usp.br

Annals of the New York Academy of Sciences
|August 30, 2005
PubMed
Summary

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Rheumatic heart disease (RHD) involves autoimmune responses to Streptococcus pyogenes. Specific streptococcal peptides and T cell reactions, particularly in heart lesions, drive RHD pathogenesis and valvular damage.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Microbiology

Background:

  • Rheumatic fever (RF) pathogenesis involves autoimmune responses to Streptococcus pyogenes.
  • CD4(+) T cells are key effectors in chronic heart lesions of rheumatic heart disease (RHD).
  • Molecular mimicry between streptococcal antigens and human tissues drives RHD.

Purpose of the Study:

  • Investigate the role of specific streptococcal antigens in RHD pathogenesis.
  • Analyze T cell responses and their migration to heart tissue in RHD patients.
  • Identify factors contributing to valvular lesions in RHD.

Main Methods:

  • T cell clone recognition of streptococcal M5(81-103) region and M5(81-96) peptide.
  • HLA-DR typing of RHD patients.

Related Experiment Videos

  • T cell repertoire analysis (BV families, TCR BVBJ, CDR3 sequences).
  • Cytokine production (TNF-alpha, IFN-gamma, IL-10, IL-4) by heart-infiltrating cells.

    • Main Results:

    • The streptococcal M5(81-103) region is recognized by intralesional and peripheral T cells.
    • Peripheral T cells from Brazilian RHD patients recognized M5(81-96) peptide, associated with HLA-DR7/DR53.
    • Oligoclonal T cell expansions were found in heart lesions, indicating preferential migration.
    • Heart-infiltrating cells produced pro-inflammatory and regulatory cytokines; valvular tissue showed limited IL-4 production.

    Conclusions:

    • The streptococcal M5(81-103) region is a potential trigger for autoimmune reactions in RHD.
    • HLA-DR7 may contribute to multiple valvular lesions in RHD.
    • Preferential T cell migration to the heart and local cytokine imbalance, especially in valves, likely drive progressive valvular damage in RHD.