ニワトリの実験的アレルギー性脳脊髄炎に関する免疫生物学的研究
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Paying attention to the ontogenetic dissociation of immunologic competence in chickens, i.e. the thymus-dependent and the bursa dependent immune systems, the author performed some experiments in an attempt to elucidate the complicated immunopathogenetic mechanism of expeimental allergic encephalomyelitis (EAE). Seven-week-old chickens were divided into five groups, which were intact normal, surgically bursectomized, hormonally bursectomized, surgically thymectomized, and given rabbit anti-thymic lymphocyte serum after surgical thymectomy, respectively. All of them were sensitized with encephalitogenic basic protein (EBP) in Freunds adjuvant. EBP had been extracted from the bovine spinal cord by Kiess method.The “bursaless” chickens lacking in humoral immunity exhibited clinical symptoms, such as ataxia and paralysis, and typical demyelinative lesions in the brain and spinal cord, showing the complete absence of anti-EBP antibody in serum with certainty. By contrast, the “thymusless” chickens devoid of cellular immunity manifested no clinical or histological evidence of EAE, in spite of the presence of serum anti-EBP antibody. It was histologically demonstrated that EAE of a “bursaless” chicken was transferred passively to another “bursaless” bird by the aid of sensitized lymphoid cells, but not to a “thymobursaless” bird. These results suggest that the thymus-dependent lymphoid cells of recipients passively sensitized with the donors sensitized cells may participate in the development of EAE.From the findings mentioned above, it was apparantly confirmed that EAE could be provoked by sensitized thymus-dependent lymphoid cells without participation of humoral anti-EBP antibody. Accordingly, the demyelination of EAE may be attributed to the glio- and myelinotoxicity of cellular antibody to EBP.