Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
DOI: 10.1017/S146239940501015X; 9 December 2005
Luiza Guilherme, Kellen Faé, Sandra E. Oshiro and Jorge Kalil (2005) Molecular pathogenesis of rheumatic fever and rheumatic heart disease.
Expert Rev. Mol. Med. Vol. 7, Issue 28, DOI: 10.1017/S146239940501015X

Molecular pathogenesis of rheumatic fever and rheumatic heart disease

Luiza Guilherme, Kellen Faé, Sandra E. Oshiro and Jorge Kalil

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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.

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Figure 1. Features of Streptococcus pyogenes.
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Figure 2. Major events triggering rheumatic heart disease lesions.
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Table 1. HLA class II alleles associated with rheumatic fever and rheumatic heart disease.
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Table 2. Crossreactivity of M-protein-reactive antibodies with human proteins.
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