PNAS：可抑制MS的调节性T细胞育成
多发性硬化症(MS)是一种自身免疫性疾病。当身体里的T细胞攻击用来隔绝大脑、脊髓和视神经的神经纤维多脂肪髓鞘时，就会产生多发性硬化症，因为缺乏保护层的神经无法在体内传送电子信号。这一疾病可以在人体内维持数十年，逐步摧毁中枢神经系统。Joel Stern领导的研究小组培育出了可以在小鼠体内抑制多发性自身免疫性疾病、包括多发性硬化症的调节性T细胞。相关论文发表在美国《国家科学院院刊》（PNAS）上。
为了培育出可以对抗多发性硬化症的T细胞，研究人员先用被称为氨基酸共聚物的化合物对小鼠进行免疫，再从它们的脾和淋巴结中培育出T细胞。这些新的T细胞系分泌出高水平的IL-10和IL-13，两者均为免疫化合物，在免疫抑制中扮演重要的角色。当这些分泌IL-10的T细胞被转移到被诱发了包括多发性硬化症在内的自身免疫性疾病的小鼠身上时，它们表现出了可以预防或减轻这类疾病的功能。（来源：EurekAlert!中文版）
生物谷推荐原始出处：
（PNAS），doi：10.1073/pnas.0712131105，Joel N. H. Stern，Jack L. Strominger
Amino acid copolymer-specific IL-10-secreting regulatory T cells that ameliorate autoimmune diseases in mice
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138
Contributed by Jack L. Strominger, December 26, 2007 (sent for review November 19, 2007)
Abstract
IL-10-secreting regulatory T cell lines specific to glatiramer acetate [poly(Y,E,A,K)n] or poly(Y,F,A,K)n have been established from the enlarged spleen and lymph nodes that result from copolymer treatment of SJL mice in which experimental autoimmune encephalomyelitis was induced by PLP139-151. These CD4+CD25+T cell lines secrete high levels of IL-10 and IL-13 but only small amounts of IL-4 and virtually no TGF-β, IL-17, IL-6, IFN-
, or TNF-
. Their phenotypes are particularly characterized by the absence of Foxp3 and the presence of two TNFR family members, CD30 and GITR. The lines proliferated specifically to the immunizing copolymers but were autoantigen-nonspecific, in that the same T cell line could suppress autoimmunity induced by three different autoantigens in SJL mice, i.e., PLP139-151(EAE), MBP85-99 (EAE), and bovine peripheral nerve myelin (experimental autoimmune neuritis), indicating they function by bystander suppression.
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