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Frontiers in Autoimmune Disease: Rheumatic Fever and Rheumatic Heart Disease

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Rheumatic heart disease is a sequel of rheumatic fever that follows an untreated group A streptococcal infection of young susceptible individuals and is considered the best model of human post-infectious autoimmune disease. Throughout the 20th century rheumatic fever’s (RF) incidence has declined in the ...

Rheumatic heart disease is a sequel of rheumatic fever that follows an untreated group A streptococcal infection of young susceptible individuals and is considered the best model of human post-infectious autoimmune disease. Throughout the 20th century rheumatic fever’s (RF) incidence has declined in the developed world, however it is still important in several developing countries. The fact that the disease leads to serious heart damage, mainly aortic and mitral valves, the number of patients with rheumatic sequels is still high in several developed countries. The disease is mediated by inflammatory and autoimmune reactions due to similarities between S. pyogenes antigens, mainly the M protein and human proteins.

Several genes related to both innate and adaptive immune responses are involved. Among the genes, those that codes for HLA class II alleles play an important role in the antigen presentation and recognition by the T-cell receptor and consequently, activation of the immune response. Both cellular and humoral immune responses take part in the autoimmune reactions, in which inflammatory cytokines are mediators of the rheumatic heart lesions. Both Th1-(IL-2, IFNγ and TNFα) and Th17-(IL-17, IL-23) cell populations are the major mediators of autoimmune reactions.

The epidemiological growth of streptococcal diseases in undeveloped and developing countries has encouraged many groups in the last 15 years, to study vaccine candidates for preventing Group A Streptococcus (GAS) infections.

A Research Topic on Rheumatic Fever / Rheumatic Heart Disease will certainly contribute to understand the autoimmune process triggered by an infectious agent and how to develop a vaccine without causing autoimmune reactions.


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