{'fraction_non_alphanumeric': 0.016008537886873, 'fraction_numerical': 0.0, 'mean_word_length': 6.0, '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}}
[Pathogenesis of multiple sclerosis and other neural autoimmune diseases].

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. Its pathological hallmark is the demyelinated plaque with reactive glial scarring. Recent neuropathological and immunopathological data suggest a pronounced pathologic heterogeneity of MS plaques. Although demyelination is present in all lesions, the extent of oligodendroglia loss, remyelination and axonal pathology is highly variable. In the present review, data are discussed on the fate of myelin forming cells in MS lesions, which suggest that fundamentally different immunological mechanisms may be involved in the formation of the lesions in different MS patients. Possible immunopathogenetic mechanisms are discussed by comparing the different types of MS lesions with those described in different experimental models of inflammatory demyelinating disease.