Lyman W D, Kadish A S, Brosnan C F, Raine C S
Cell Immunol. 1983 May;78(1):43-55. doi: 10.1016/0008-8749(83)90258-7.
Random-bred Hartley and inbred Strain 2 and Strain 13 guinea pigs were inoculated for acute experimental autoimmune encephalomyelitis (EAE). Sixty-six percent (69/103) of the Hartleys developed signs of EAE while the remaining 34% (34/103) were resistant. No Strain 2 and all Strain 13 guinea pigs developed EAE. Histologic examination of nervous tissue revealed that susceptible Hartleys and Strain 13 and Strain 2 animals had lesions characteristic of EAE. Tissue from resistant Hartleys showed fewer and less severe changes. Lymphocyte-transformation assays with EAE-inducing and noninducing antigens and T-cell mitogens revealed three different sets of responses in vitro: (i) lymphocytes from all animals responded to mitogens; (ii) lymphocytes from susceptible animals responded to EAE-inducing antigens; and (iii) lymphocytes from resistant Hartleys were suppressed from responding to the mitogens solely by EAE-inducing antigens. Plasmas from all EAE-sensitized animals had equivalent anti-myelin basic proteins (MBP) antibody titers and skin tests of EAE-inoculated Hartleys were all positive for MBP sensitization. Therefore, resistance and reduced histologic changes characteristic of EAE correlated with a disease-specific antigen-induced suppression of lymphocyte responses to T-cell mitogens. This suggests that clinical resistance to EAE in Hartley guinea pigs is mediated by an immunologic suppressor mechanism.
将随机繁殖的哈特利豚鼠以及近交系2和近交系13豚鼠接种，以诱发急性实验性自身免疫性脑脊髓炎（EAE）。66%（69/103）的哈特利豚鼠出现了EAE症状，而其余34%（34/103）具有抗性。近交系2豚鼠无一发病，所有近交系13豚鼠均患上了EAE。对神经组织进行组织学检查发现，易感的哈特利豚鼠以及近交系13和近交系2豚鼠具有EAE的特征性病变。抗性哈特利豚鼠的组织变化较少且不太严重。用诱发EAE和不诱发EAE的抗原以及T细胞有丝分裂原进行淋巴细胞转化试验，结果显示体外有三种不同的反应：（i）所有动物的淋巴细胞对有丝分裂原均有反应；（ii）易感动物的淋巴细胞对诱发EAE的抗原起反应；（iii）抗性哈特利豚鼠的淋巴细胞仅被诱发EAE的抗原抑制，无法对有丝分裂原起反应。所有致敏EAE动物的血浆具有相当的抗髓鞘碱性蛋白（MBP）抗体滴度，接种EAE的哈特利豚鼠的皮肤试验对MBP致敏均呈阳性。因此，EAE抗性及相关组织学变化减少与疾病特异性抗原诱导的淋巴细胞对T细胞有丝分裂原反应的抑制相关。这表明哈特利豚鼠对EAE的临床抗性是由一种免疫抑制机制介导的。
