The involvement of T cells in the pathogenesis of human autoimmune disease has long been suspected, even though few data are available that directly implicate these T cells. In contrast, antigen-specific CD4+ T cells have clearly been demonstratedto induce autoimmune tissue destruction and clinical disease in experimental animal models. These pathogenic T cells retained the tendency to develop characteristic CDR3 "motifs" specific for target peptides, as well as to utilize common V gene families. This knowledge has led to immune interventions directed at both clonotypic CDR3 determinants present on only the peptide-specific T cells and more broadly represented V gene determinants, typically the CDR1, CDR2, and FW3 loops of the TCR.
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