Molecular mimicry in the autoimmune pathogenesis of rheumatic heart disease.
Molecular mimicry is a hallmark of the pathogenesis of rheumatic fever where the streptococcal group A carbohydrate epitope, N-acetyl glucosamine, and the a-helical coiled-coil streptococcal M protein structurally mimic cardiac myosin in the human disease, rheumatic carditis, and in animal models immunized with streptococcal M protein and cardiac myosin. Recent studies have unraveled the potential pathogenic mechanisms by which the immune response against the group A streptococcus attacks the rheumatic valve leading to chronic rheumatic heart disease. Both B- and T-cell responses are involved in the process, and evidence for the hypotheses of molecular mimicry and epitope spreading are reviewed.
Guilherme
Luiza
L
Heart Institute-InCor, University of São Paulo, School of Medicine, São Paulo, Brazil.
Kalil
Jorge
J
Cunningham
Madeleine
M
D000818:Animals; D001327:Autoimmune Diseases; D006801:Humans; D018716:Molecular Mimicry / Q000276:immunology*; D012214:Rheumatic Heart Disease / Q000209:etiology* / Q000276:immunology*