Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein. II. Suppression of disease and in vitro immune responses is mediated by antigen-specific CD8+ T lymphocytes.
Suppression of experimental autoimmune encephalomyelitis by oral administration of myelin basic protein. II. Suppression of disease and in vitro immune responses is mediated by antigen-specific CD8+ T lymphocytes.
复制标题
口服髓磷脂碱性蛋白抑制实验性自身免疫性脑脊髓炎。
DOI：
10.4049/jimmunol.142.3.748
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发表时间：
1989
影响因子：
4.4
通讯作者：
H. Weiner
中科院分区：
文献类型：
--
作者：
O. Lider;L. B. Santos;C. S. Lee;P. Higgins;H. Weiner
我们之前已经证明，口服豚鼠髓磷脂碱性蛋白（MBP）可以保护Lewis大鼠，当随后用CFA中的豚鼠髓磷脂碱性蛋白（MBP）免疫时，避免诱导实验性自身免疫性脑脊髓炎（EAE）。此外，口服MBP 耐受的动物对MBP 的增殖和抗体反应也减弱，但对其他Ag 的反应没有减弱。尽管如此，EAE 模型中 MBP 口服耐受的机制仍不清楚。在本研究中，我们报告从 MBP 口服耐受动物的脾脏和肠系膜淋巴结中分离的 T 细胞可以过继转移针对 EAE 的保护作用。此外，这些 T 细胞属于 CD8+ 亚类。此外，来自口服 MBP 耐受动物的 CD8+ T 细胞也以 Ag 特异性方式抑制体外增殖反应和对 MBP 的抗体反应。这些结果表明，口服自身抗原后会启动活性细胞机制，从而下调实验性自身免疫性疾病，并为介导体内和体外抑制的细胞的分离和表征提供基础。
We have previously demonstrated that the oral administration of guinea pig myelin basic protein (MBP) protects Lewis rats against the induction of experimental autoimmune encephalomyelitis (EAE) when subsequently immunized with guinea pig MBP in CFA. In addition, animals made orally tolerant to MBP also have diminished proliferative and antibody responses to MBP, but not to other Ag. Nonetheless, the mechanism of oral tolerance to MBP in the EAE model remains undefined. In the present study, we report that T cells isolated from the spleen and mesenteric lymph nodes of MBP orally tolerized animals can adoptively transfer protection against EAE. Furthermore, these T cells are of the CD8+ subclass. In addition, CD8+ T cells from MBP orally tolerized animals also suppress in vitro proliferative responses and antibody responses to MBP in an Ag-specific fashion. These results demonstrate that active cellular mechanisms are initiated after oral administration of an autoantigen that can down-regulate an experimental autoimmune disease and provide the basis for the isolation and characterization of the cells mediating both in vivo and in vitro suppression.