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Revisiting the pathogenesis of rheumatic fever and carditis

Rajendra Tandon1, Meenakshi Sharma, Y Chandrashekhar

  • 1Sitaram Bhartia Institute of Science and Research, B-16, Mehrauli Institutional Area, New Delhi 110016, India.

Nature Reviews. Cardiology
|January 16, 2013
PubMed

Insights

Rheumatic fever pathogenesis may involve streptococcal M protein binding to collagen type IV, initiating an antibody response to collagen. This suggests collagen, not molecular mimicry, is key in rheumatic fever development.

Area of Science:

  • Immunology
  • Rheumatology
  • Pathogenesis of Infectious Diseases

Background:

  • Rheumatic fever pathogenesis is poorly understood, with research focusing on streptococcal M protein cross-reactivity.
  • Current hypotheses suggest molecular mimicry between streptococcal M protein and host tissues.
  • Pathological findings indicate subendothelial and perivascular connective tissue damage.

Approach:

  • Investigating the interaction between streptococcal M protein N-terminus and collagen type IV CB3 region.
  • Analyzing the resulting antibody response to collagen.
  • Comparing the proposed mechanism with collagen involvement in other autoimmune diseases.

Key Points:

  • Streptococcal M protein N-terminus binds to collagen type IV CB3 region.
  • This interaction triggers an antibody response targeting collagen, leading to inflammation.
  • The antibodies generated do not cross-react with streptococcal M protein.

Conclusions:

  • The proposed mechanism challenges the molecular mimicry hypothesis in rheumatic fever.
  • This alternative hypothesis implicates collagen type IV and associated autoimmune responses.
  • Findings suggest potential links to Goodpasture and Alport syndromes due to shared collagen involvement.

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