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- W2003994310 abstract "Molecular mimicry was proposed as a potential mechanism for streptococcal sequelae leading to rheumatic fever (RF) and rheumatic heart disease (RHD). CD4(+)infiltrating T cells are able to recognize streptococcal M peptides and heart tissue proteins. We analyzed the M5 peptide- and heart-specific responses, cytokine profile and T cell receptor (TCR) BV usage from peripheral and heart-infiltrating T cell lines and clones from patients across the clinical spectrum of ARF/RHD. The patient with ARF displayed a higher frequency of mitral valve infiltrating T cell clones reactive against M5: 1-25, 81-103 and 163-177 regions and several valve-derived proteins than the post-RF and chronic RHD patient (67%; 20% and 27%, respectively). The presence of oligoclonal BV families indicative of oligoclonal T cell expansion among mitral valve-derived T cell lines was increased in the chronic RHD patient. Furthermore, mitral valve T cell lines from all patients produced significant amounts of inflammatory cytokines interferon-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNFalpha) in response to M5(81-96) peptide, with the highest production attained by the chronic RHD patient. These data are consistent with an important role for M5 peptide and host antigen-driven, T1-type CD4(+)T cells in the pathogenesis of RHD and heart lesion progression after recurrence of the streptococcal infection." @default.
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- W2003994310 date "2001-05-01" @default.
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- W2003994310 title "Heart-directed Autoimmunity: the Case of Rheumatic Fever" @default.
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- W2003994310 doi "https://doi.org/10.1006/jaut.2000.0487" @default.
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