We propose a framework to explain how T cells achieve specificity and sensitivity, how the affinity of the TcR peptide/MHC interaction controls positive and negative thymic selection and mature T cell survival, and whether antigen-dependent activation and inactivation takes place. Two distinct types of signalling can lead to mature T cell multiplication. One requires the TcR to recognize with a certain affinity an antigen-derived peptide, an agonist peptide, bound to an MHC molecule. The other, the tonic signal, leads to naïve T cell survival and modest proliferation if the T cell successfully competes for endogenous, self-peptide/MHC ligands, involving lower affinity TCR/ligand interactions. Many suggest lymphopenia contributes to autoimmunity by increasing the strength of TcR-tonic signalling, and so activation of anti-self T cells. We suggest T cell activation requires antigen-mediated cooperation between T cells. Increased tonic signalling under lymphopenic conditions facilitates T cell proliferation and so antigen-dependent cooperation and activation of anti-self T cells.

中文翻译：

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在T细胞发育上，淋巴细胞减少有助于T细胞信号，T细胞特异性和敏感性以及自身免疫性。

我们提出了一个框架来解释T细胞如何实现特异性和敏感性，TcR肽/ MHC相互作用的亲和力如何控制正，负胸腺选择和成熟的T细胞存活，以及是否发生抗原依赖性激活和失活。两种不同类型的信号传导可导致成熟的T细胞繁殖。一个要求TcR以某种亲和力识别与MHC分子结合的抗原衍生肽，激动剂肽。如果T细胞成功竞争内源性自身肽/ MHC配体，涉及较低亲和力的TCR /配体相互作用，则另一个信号即补品信号将导致幼稚的T细胞存活和适度的增殖。许多人认为淋巴细胞减少症可通过增加TcR张力信号的强度来促进自身免疫，从而激活抗自身T细胞。我们建议T细胞激活需要T细胞之间的抗原介导的合作。在淋巴细胞减少的条件下增加的滋补信号传导促进T细胞增殖，因此抗原依赖的协同作用和抗自身T细胞的活化。