The syngeneic T-T lymphocyte reaction (STTLR). I. Induction of primary T anti-T cell proliferative responses in T cell cultures stimulated with self- and antigen-reactive T cells.

H Suzuki, B Evavold, T J Swartz, S L Latta, J Quintáns
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Abstract

The generally accepted "Gershonian" view of immunoregulation attributes T cell-mediated regulation of immune responses to the activities of discrete T cell subsets with specialized functions such as help, suppression, and contrasuppression. Several observations made in our laboratory are not compatible with this paradigm. For instance, careful quantitations of carrier-specific T cell help to hapten-specific B cells in an adoptive transfer system yielded complex dose-response curves that could not be explained on the basis of interactions between discrete subsets of helper and suppressor cells. Rather, the results were most easily interpreted according to a model based on the following assumptions: (1) Regulation of helper T cell activity is a dose-dependent, dynamic property of T cell populations that exhibit a high degree of connectivity (self-recognition) and (2) helper T cells have the ability to perform different functions, depending on the current activity of other interacting lymphocytes. A good example of cloned T cells capable of performing multiple immunoregulatory functions was provided by the IEk-specific self-reactive Lbd line which provided help, suppression, and contrasuppression to T cell dependent PFC responses (see Quintáns et al., 1986). Since these effects were strictly dependent on the levels of antigen-specific T cell help, we hypothesized that Lbd cells interacted with other T cells to modulate their function. In this paper, we directly test the hypothesis that activated T cells can interact directly with resting T cells and describe the proliferative component of a syngeneic T cell anti-T cell response induced by antigen and self-reactive helper and cytotoxic T cells. In a follow-up report, we will describe the effector component of the T anti-T cell response.(ABSTRACT TRUNCATED AT 400 WORDS)

同基因t淋巴细胞反应(STTLR)。在自体和抗原反应性T细胞刺激的T细胞培养中诱导原代T抗T细胞增殖反应。
普遍接受的“Gershonian”免疫调节观点将T细胞介导的免疫反应调节归因于具有特殊功能(如帮助、抑制和反抑制)的离散T细胞亚群的活动。在我们的实验室中所做的一些观察与这种范式不相容。例如,在过继性转移系统中,仔细定量的载体特异性T细胞有助于半抗原特异性B细胞产生复杂的剂量-反应曲线,这无法根据辅助细胞和抑制细胞的离散亚群之间的相互作用来解释。相反,根据基于以下假设的模型,结果最容易解释:(1)辅助性T细胞活性的调节是一种剂量依赖的、表现出高度连通性(自我识别)的T细胞群的动态特性;(2)辅助性T细胞有能力执行不同的功能,这取决于其他相互作用淋巴细胞的当前活性。克隆T细胞能够执行多种免疫调节功能的一个很好的例子是iek特异性自反应性Lbd系,它对T细胞依赖性PFC反应提供了帮助、抑制和反抑制(见Quintáns等人,1986)。由于这些作用严格依赖于抗原特异性T细胞帮助的水平,我们假设Lbd细胞与其他T细胞相互作用以调节其功能。在本文中,我们直接验证了激活的T细胞可以直接与静止T细胞相互作用的假设,并描述了由抗原和自反应性辅助T细胞和细胞毒性T细胞诱导的同源T细胞抗T细胞反应的增殖成分。在后续报告中,我们将描述T抗T细胞反应的效应成分。(摘要删节为400字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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