{'fraction_non_alphanumeric': 0.013852813852813853, 'fraction_numerical': 0.0, 'mean_word_length': 5.282608695652174, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Infection and multiple sclerosis].

Multiple sclerosis is a putative autoimmune disease in which limited numbers of autoimmune T cells reactive to myelin basic protein or proteolipid protein would play critical roles in initiation or augmentation of the inflammatory processes. Owing to the recent immunological studies, it is now possible to discuss the possible link between infectious agents and the development of MS on the molecular terms. This article deals with key issues in this subject such as molecular mimicry between autoantigen and viral peptide, autoimmune T cell stimulation by bacterial superantigens, and regulatory network in MS. In addition to reviewing the current activity in other laboratories, I point out that there might be much more broader range of peptide ligands for autodestructive T cells causing MS. This postulate is based on our recent discovery for the presence of degenerate autoimmune T cells in animal model of MS (EAE). I also indicate the possibility that immune regulatory system could be destroyed by some infectious agents. These informations should have significant implications for management of MS patients.