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Molecular pathogenesis of rheumatic fever and rheumatic heart disease

Luiza Guilherme1, Kellen Faé, Sandra E Oshiro

  • 1Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, 05403-000 SP, Brazil. luizagui@usp.br

Expert Reviews in Molecular Medicine
|December 13, 2005
PubMed

Insights

Rheumatic heart disease (RHD) may stem from molecular mimicry between streptococcal and human proteins. Immune responses, particularly T helper 1 (Th1) cytokines, appear to drive RHD heart lesions, with a lack of interleukin 4 (IL-4) potentially worsening them.

Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Infectious Disease

Background:

  • Rheumatic fever (RF) and rheumatic heart disease (RHD) are autoimmune conditions potentially triggered by molecular mimicry between streptococcal and human proteins.
  • Genetic factors may influence an individual's susceptibility to developing RF/RHD.

Purpose of the Study:

  • To summarize studies on genetic susceptibility markers for RF/RHD.
  • To investigate the role of molecular mimicry in RHD pathogenesis, focusing on cellular and molecular mechanisms.
  • To assess the involvement of T helper 1 (Th1) and T helper 2 (Th2) cytokine profiles in RHD lesion development.

Main Methods:

  • Review of studies on genetic susceptibility in RF/RHD.
  • Analysis of B and T cell responses to streptococcal antigens and human tissue proteins in RF/RHD patients.
  • Assessment of T cell recognition of heart-crossreactive antigens.
  • Measurement of cytokine production by peripheral blood mononuclear cells and heart-infiltrating mononuclear cells.

Main Results:

  • Molecular mimicry between streptococcal and human proteins is implicated in RHD.
  • T cells infiltrating heart lesions and peripheral blood cells show responses to streptococcal antigens and human proteins.
  • Th1-type cytokines are identified as mediators of RHD heart lesions.
  • An insufficient presence of interleukin 4 (IL-4)-producing cells in valvular tissue may contribute to lesion progression.

Conclusions:

  • Molecular mimicry and specific immune responses drive RHD pathogenesis.
  • Th1 cytokines play a key role in mediating RHD heart lesions.
  • Imbalances in cytokine production, specifically a deficit in IL-4, may exacerbate valvular damage in RHD.

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