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Molecular pathogenesis of rheumatic fever and rheumatic heart disease

Published online by Cambridge University Press:  08 December 2005

Luiza Guilherme
Affiliation:
Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, 05403-000 SP, Brazil.
Kellen Faé
Affiliation:
Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, 05403-000 SP, Brazil.
Sandra E. Oshiro
Affiliation:
Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, 05403-000 SP, Brazil.
Jorge Kalil
Affiliation:
Department of Clinical Medicine, Clinical Hospital and Heart Institute (InCor), School of Medicine, University of São Paulo, São Paulo, 05403-000 SP, Brazil.

Abstract

Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). This article summarises studies on genetic susceptibility markers involved in the development of RF/RHD. It also focuses on the molecular mimicry in RHD mediated by the responses of B and T cells of peripheral blood, and T cells infiltrating heart lesions, against streptococcal antigens and human tissue proteins. The molecular basis of T-cell recognition is assessed through the definition of heart-crossreactive antigens. The production of cytokines from peripheral and heart-infiltrating mononuclear cells suggests that T helper 1 (Th1)-type cytokines are the mediators of RHD heart lesions. An insufficiency of interleukin 4 (IL-4)-producing cells in the valvular tissue might contribute to the maintenance and progression of valve lesions.

Type
Review Article
Copyright
© Cambridge University Press 2005

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