{'fraction_non_alphanumeric': 0.023863636363636365, 'fraction_numerical': 0.009659090909090909, 'mean_word_length': 6.246913580246914, '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}}
Interleukin‐10 prevents experimental allergic encephalomyelitis in rats

Experimental allergic encephalomyelitis (EAE) is an autoimmune disease mediated by myelin protein‐specific CD4+ T lymphocytes of the Th1‐like phenotype. In rats, the disease is characterized by a monophasic clinical manifestation, followed by a subsequent spontaneous remission and the establishment of life‐long resistance to reinduction of disease. Recent data indicate that intracerebral cytokine production, in particular synthesis of interleukin(IL)‐10, is selectively up‐regulated during the recovery phase of disease. This led us to assess the effects of IL‐10 on different rat lymphoid cell functions in vitro and to consider the possibility of an IL‐10‐mediated treatment to prevent the induction of central nervous system (CNS) autoimmune disease in vivo. Human recombinant IL‐10 suppressed interferon‐γ induced major histocompatibility complex class II up‐regulation in rat peritoneal macrophages, exhibited pleiotropic effects on thymocytes and totally abrogated tumor necrosis factor production of encephalitogenic T lymphocytes in vitro, without simultaneously affecting proliferative responses of the cells. Upon systemic administration during the initiation phase of disease, IL‐10 was effective in markedly suppressing the subsequent induction of EAE in Lewis rats. This suppression of clinical disease coincided with a significant and specific elevation of myelin basic protein‐specific autoantibody production, a sustained T cell proliferative response to myelin basic protein and a diminution of CNS infiltrations and thymic involutions in diseased animals. These data implicate IL‐10 as a possible candidate for treatment of Th1‐mediated CNS (auto‐) immune diseases.