id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-009570-djxoiytq	Gran, Bruno	Molecular mimicry and multiple sclerosis: Degenerate T‐cell recognition and the induction of autoimmunity	2001-06-01		.txt	text/plain	5335	274	40	Both clinical and experimental evidence supports the hypothesis that immune mechanisms are involved in the pathogenesis of inflammatory demyelination in multiple sclerosis (MS) and that autoreactive T lymphocytes initiate the process of central nervous system (CNS) myelin damage. This disease model has provided insight into the pathogenic "steps" that may be relevant to MS, including (1) genetic susceptibility, (2) priming and activation of myelin-specific T cells, (3) interaction of autoreactive T cells with endothelium and migration into the CNS, and (4) recognition of myelin antigens and initiation of inflammatory or demyelinating damage (Fig 1) . 44, 45 Molecular mimicry motifs that would satisfy both MHC binding and recognition by specific TCR were used by Wucherpfennig and Strominger 46 to identify microbial peptides that were effective in activating three MBPspecific T-cell clones (TCCs) derived from MS patients (Table 1) . Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein	./cache/cord-009570-djxoiytq.txt	./txt/cord-009570-djxoiytq.txt