Moser M, Mizuochi T, Sharrow S O, Singer A, Shearer G M
J Immunol. 1987 Mar 1;138(5):1355-62.
Hybrid mice of the (B6 X bm12)F1 combination were inoculated i.v. with parental B6 spleen cells to induce a class II graft-vs-host disease (GVH). Such mice failed to generate in vitro cytotoxic T lymphocyte (CTL) responses that were dependent upon L3T4+ T helper cell (Th) function (e.g., anti-B6-TNP) but were capable of generating in vitro CTL responses that could be mediated by Lyt-2+ Th cells (anti-allo class I). When Th function was assayed directly by interleukin 2 (IL 2) secretion, class II GVH animals were found to be deficient in L3T4+ but not Lyt-2+ IL 2-secreting Th cells. This selective deficiency in L3T4+ Th function correlates with a selective decrease in class II GVH mice of host-derived derived L3T4+ T cells. In addition, it was found that the spleens of class II GVH mice contained cells capable of selectively suppressing L3T4+ Th function. In contrast, mice in which a class I + II GVH occurred were depleted of both L3T4+ and Lyt-2+ Th function as assessed by IL 2 production. The findings that class II GVH selectively depletes L3T4+ T cells and T cell functions are discussed with respect to the immune function of distinct T cell subsets in normal and diseased states.
将(B6 X bm12)F1组合的杂种小鼠经静脉注射亲代B6脾细胞,以诱导II类移植物抗宿主病(GVH)。这类小鼠无法产生依赖L3T4 + T辅助细胞(Th)功能的体外细胞毒性T淋巴细胞(CTL)反应(例如,抗B6-TNP),但能够产生可由Lyt-2 + Th细胞介导的体外CTL反应(抗同种异体I类)。当通过白细胞介素2(IL 2)分泌直接检测Th功能时,发现II类GVH动物的L3T4 +但不是Lyt-2 +分泌IL 2的Th细胞存在缺陷。L3T4 + Th功能的这种选择性缺陷与宿主来源的L3T4 + T细胞在II类GVH小鼠中的选择性减少相关。此外,还发现II类GVH小鼠的脾脏中含有能够选择性抑制L3T4 + Th功能的细胞。相比之下,通过IL 2产生评估,发生I + II类GVH的小鼠的L3T4 +和Lyt-2 + Th功能均被耗尽。就正常和疾病状态下不同T细胞亚群的免疫功能而言,讨论了II类GVH选择性消耗L3T4 + T细胞和T细胞功能的发现。