{'fraction_non_alphanumeric': 0.019455252918287938, 'fraction_numerical': 0.0, 'mean_word_length': 5.9192825112107625, '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}}
Serum IgM repertoire reactions to MBP/CFA immunization reflect the individual status of EAE susceptibility.

Lewis rats develop experimental allergic encephalomyelitis (EAE) in response to immunization with myelin basic protein (MBP) in CFA, while Fischer rats are usually resistant. These strains, while comparably producing anti-MBP antibodies, also differ in their repertoire reactions to immunization, as measured by patterns of serum IgM reactivity with various autologous proteins. We have now scored IgM repertoire reactions to MBP/CFA immunization after treatments that alter EAE susceptibility in either strain. The results show that abrogation of EAE susceptibility in Lewis rats by a previous experience of T cell-induced passive EAE provoked a novel set of IgM reactivities that otherwise characterized the Fischer's repertoire reaction. Conversely, these reactivities were delayed in the response of Fischer rats that had been rendered EAE-susceptible by cyclophosphamide. Another IgM reactivity with a significant association to individual EAE severity in Lewis rats behaved reciprocally. Together with previous results, these observations suggest that putative regulatory mechanisms concordantly affect EAE resistance and IgM repertoire reactions, operating naturally in Fischer rats and abrogatable by cyclophosphamide treatment, whereas naturally suppressed, but restorable in Lewis rats. Other treatments altering EAE susceptibility, however, did not share these characteristics and may thus be mediated by other mechanisms.