由共聚物1诱导的Th2型T细胞系和克隆对实验性自身免疫性脑脊髓炎的旁观者抑制作用
Bystander suppression of experimental autoimmune encephalomyelitis by T cell lines and clones of the Th2 type induced by copolymer 1.
作者信息
Aharoni R, Teitelbaum D, Sela M, Arnon R
机构信息
Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel.
出版信息
J Neuroimmunol. 1998 Nov 2;91(1-2):135-46. doi: 10.1016/s0165-5728(98)00166-0.
The synthetic amino acid copolymer, copolymer 1 (Cop 1) induces T suppressor (Ts) lines/clones, which are confined to the Th2 pathway, cross react with myelin basic protein (MBP), but not with other myelin antigens on the level of Th2 cytokine secretion. Nevertheless, Cop 1 Ts cells inhibited the IL-2 response of a proteolipid protein (PLP) specific line. Furthermore, Cop 1 Ts cells ameliorated EAE induced by two unrelated encephalitogenic epitopes of PLP: p139-151 and p178-191, that produced different forms of disease. This bystander suppression demonstrated by the Cop 1 Ts cells may explain the therapeutic effect of Cop 1 in EAE and MS.
合成氨基酸共聚物，即共聚物1（Cop 1）可诱导T抑制细胞（Ts）系/克隆，这些细胞局限于Th2途径，在Th2细胞因子分泌水平上与髓鞘碱性蛋白（MBP）发生交叉反应，但不与其他髓鞘抗原发生交叉反应。然而，Cop 1 Ts细胞抑制了脂蛋白（PLP）特异性系的IL-2反应。此外，Cop 1 Ts细胞改善了由PLP的两个不相关的致脑炎表位：p139 - 151和p178 - 191诱导的实验性自身免疫性脑脊髓炎（EAE），这两个表位产生了不同形式的疾病。Cop 1 Ts细胞所表现出的这种旁观者抑制作用可能解释了Cop 1在EAE和多发性硬化症（MS）中的治疗效果。
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