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三硝基苯基反应性细胞毒性效应系统的体内启动研究。III. 辅助性T细胞是否参与交叉反应性以及限制性细胞毒性反应的体外产生?

Studies on in-vivo priming of the trinitrophenyl-reactive cytotoxic effector-system. III. Are helper T cells involved in the in-vitro generation of cross-reactive as well as restricted cytotoxic responses?

作者信息

Fujiwara H, Levy R B, Shearer G M

出版信息

Immunobiology. 1982 Feb;160(5):472-8. doi: 10.1016/s0171-2985(82)80009-0.

Abstract

The present study investigates the role of helper cells from trinitrophenyl(TNP)-primed mice in the generation of cytotoxic T lymphocytes (CTL) which lyse TNP-modified syngeneic (TNP-self) targets and cross-reactively lyse TNP-allogeneic target cells. Anti-TNP CTL activities generated from primed (either by intraperitoneal injection of TNP-syngeneic cells or by skin painting with trinitrochlorobenzene) and unprimed spleen cells were compared. When effector populations with comparable lytic activities on TNP-self targets were tested against allogeneic TNP-modified targets, only the in vivo primed effector cells displayed significant cytotoxicity. Since radioresistant helper cells have been found to enhance the anti-TNP-self CTL response, the question was raised whether this helper population could be shown to be involved in the enhanced TNP-allogeneic cross-reactive lysis. Normal spleen cells co-cultured with radioresistant helper cells failed to induce any detectable lysis on TNP-allogeneic targets under conditions for which these helper cells did enhance the lysis detected on TNP-self targets. These results suggest that triggering of such TNP-cross-reactive effector cells during the in vivo priming stage is responsible for the in vitro generation of cross-reactivity.

摘要

本研究调查了来自三硝基苯(TNP)致敏小鼠的辅助细胞在细胞毒性T淋巴细胞(CTL)产生过程中的作用,这些CTL可裂解TNP修饰的同基因(TNP-自身)靶细胞,并交叉反应性地裂解TNP-异基因靶细胞。比较了由致敏(通过腹腔注射TNP-同基因细胞或用三硝基氯苯皮肤涂抹)和未致敏的脾细胞产生的抗TNP CTL活性。当测试对TNP-自身靶细胞具有可比裂解活性的效应细胞群体对异基因TNP修饰靶细胞的作用时,只有体内致敏的效应细胞表现出显著的细胞毒性。由于已发现辐射抗性辅助细胞可增强抗TNP-自身CTL反应,因此提出了一个问题,即是否可以证明这种辅助细胞群体参与了增强的TNP-异基因交叉反应性裂解。在这些辅助细胞确实增强了对TNP-自身靶细胞检测到的裂解的条件下,与辐射抗性辅助细胞共培养的正常脾细胞未能在TNP-异基因靶细胞上诱导任何可检测到的裂解。这些结果表明,在体内致敏阶段触发此类TNP交叉反应性效应细胞是体外产生交叉反应性的原因。

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