辅助T细胞克隆产生抗原特异性分子(T- abm),其作用是诱导抑制。

D R Green, B Chue, H G Zheng, T A Ferguson, K D Beaman, P M Flood
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引用次数: 0

摘要

在Ly-1+、2-T细胞中,似乎有两种独立的抗原识别模式。辅助性和细胞毒性Ly-1 T细胞仅在I区产物的背景下识别抗原,而调节性T细胞,如T抑制诱导细胞,产生抗原特异性,抗原结合分子(T- abm)。这些T-ABM经常被发现形成生物活性的一部分,抗原特异性调节因子。许多环境条件影响外来抗原是产生导致免疫的积极反应还是产生导致耐受的消极反应。许多有利于诱导抑制性T细胞的条件同时阻碍了抗原提呈细胞与辅助性T细胞的适当相互作用。这种相似性使我们不禁要问,辅助性T细胞是否至少具有两种明显相反的功能:a)在有利于免疫的条件下,辅助性T细胞产生淋巴因子来激活免疫效应细胞;b)在有利于抑制的条件下,它们产生抑制细胞诱导的分子。因此,这个问题与免疫反应转换为积极(帮助)或消极(抑制)轨道的机制有关。此外,它开始解决辅助性T细胞与T抑制诱导细胞表现出的不同抗原识别模式之间的关系(见上文)。为了探索这个问题,我们采用抗原特异性,I-Ak限制性辅助性T细胞克隆作为辅助性T细胞的最纯粹的可用来源。我们在有利于抑制而不是帮助的条件下(例如,通过抗原呈递细胞的紫外线照射)将抗原呈递到克隆的T细胞,并在48小时后收集上清。然后在抗原特异性抑制因子的功能分析中检查上清液的活性。我们的结果表明,在有利于抑制的条件下,T-ABM在体外具有抗原特异性诱导抑制的功能。T- abm具有与辅助T细胞相同的抗原特异性,因此可能来源于克隆。这一观察结果引入了一种可能性,即抗原提呈细胞和辅助T细胞之间的相互作用是免疫反应的一个关键决定点,可以导致免疫或抑制。后者将通过辅助T细胞产生T抑制诱导因子(即T- abm)的抗原特异性成分来实现。讨论了T- abms与T细胞受体之间可能的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A helper T cell clone produces an antigen-specific molecule (T-ABM) which functions in the induction of suppression.

Among Ly-1+,2-T cells there appears to be two independent modes of antigen recognition. Helper and cytotoxic Ly-1 T cells recognize antigen only in the context of I region products whereas regulatory T cells, such as T suppressor inducer cells, produce antigen-specific, antigen-binding molecules (T-ABM). These T-ABM often have been found to form a part of biologically active, antigen-specific regulatory factors. A number of environmental conditions effect whether a foreign antigen will produce a positive response leading to immunity or a negative one leading to tolerance. Many of the conditions which favor the induction of suppressor T cells simultaneously preclude the proper interaction of antigen presenting cells with helper T cells. This parallel led us to ask whether helper T cells perform at least two, apparently opposite functions: a) under conditions favoring immunity helper T cells produce lymphokines to activate immune effector cells, and b) under conditions favoring suppression they produce molecules which function in suppressor cell induction. Therefore, this question relates to the mechanisms by which an immune response is switched into either a positive (help) or negative (suppressive) track. In addition, it begins to address the relationship between the different modes of antigen recognition exhibited by helper T cells vs. T suppressor inducer cells (see above). To explore this problem we employed an antigen-specific, I-Ak restricted helper T cell clone as the purest available source of helper T cells. We presented antigen to the cloned T cells under conditions which favor suppression rather than help (for example, by ultraviolet irradiation of the antigen-presenting cells) and collected supernatants 48 hrs later. The supernatants were then examined for activity in a functional assay for antigen-specific suppressor factors. Our results indicate that under conditions favoring suppression, a T-ABM was produced which functioned in the antigen-specific induction of suppression in vitro. The T-ABM had the same antigen specificity as that exhibited by the helper T cell and was therefore probably derived from the clone. This observation introduces the possibility that the interaction between antigen-presenting cells and helper T cells is a crucial decision point in the immune response which can lead to either immunity or suppression. The latter would be achieved through the production, by helper T cells, of an antigen-specific component of T suppressor inducer factor (i.e., the T-ABM). The possible relationship between T-ABMs and the T cell receptor is discussed.

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