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分泌2型细胞因子的CD8(+) T细胞在抵抗病毒感染的保护作用方面存在缺陷。

CD8(+) T cells secreting type 2 lymphokines are defective in protection against viral infection.

作者信息

Wirth S, van den Broek M, Frossard C P, Hügin A W, Leblond I, Pircher H, Hauser C

机构信息

Allergy Unit, Division of Immunology and Allergy, Hôpital Cantonal Universitaire, Geneva, Switzerland.

出版信息

Cell Immunol. 2000 May 25;202(1):13-22. doi: 10.1006/cimm.2000.1639.

Abstract

Effector T cells secreting type 1 and/or type 2 lymphokines (Tc1, Tc0, Tc2) were generated in vitro from CD8(+) T cells of mice with a transgenic TCR recognizing lymphocytic choriomeningitis virus (LCMV) glycoprotein to compare their effector function in vitro and in vivo. Tc1, Tc2, and Tc0 showed similar Fas- and perforin-mediated cytotoxicity in vitro. Upon adoptive transfer, Tc2 and Tc0 effectors were less efficient than Tc1 at controlling LCMV or recombinant vaccinia virus expressing the LCMV glycoprotein in vivo. Tc2 and Tc0 had decreased surface VLA-4 density and deficient activation-induced LFA-1/ICAM-1-dependent homotypic adhesion in vitro. Therefore, the reduced antiviral activity in vivo of Tc2 and Tc0 compared with Tc1 is not due to reduced cytotoxic activity or IFN-gamma secretion but may be explained by defective homing to the target organ due to decreased expression and/or lower activity of adhesion molecules.

摘要

从具有识别淋巴细胞性脉络丛脑膜炎病毒(LCMV)糖蛋白的转基因TCR的小鼠的CD8(+) T细胞中体外产生分泌1型和/或2型淋巴因子的效应T细胞(Tc1、Tc0、Tc2),以比较它们在体外和体内的效应功能。Tc1、Tc2和Tc0在体外显示出相似的Fas和穿孔素介导的细胞毒性。过继转移后,在体内控制LCMV或表达LCMV糖蛋白的重组痘苗病毒方面,Tc2和Tc0效应细胞比Tc1效率更低。Tc2和Tc0在体外表面VLA-4密度降低,且活化诱导的LFA-1/ICAM-1依赖性同型黏附存在缺陷。因此,与Tc1相比,Tc2和Tc0在体内抗病毒活性降低并非由于细胞毒性活性降低或IFN-γ分泌减少,而是可能由于黏附分子表达降低和/或活性较低导致归巢至靶器官存在缺陷所致。

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