Intrinsic CD4+ T cell sensitivity and response to a pathogen are set and sustained by avidity for thymic and peripheral complexes of self peptide and MHC.
Intrinsic CD4+ T cell sensitivity and response to a pathogen are set and sustained by avidity for thymic and peripheral complexes of self peptide and MHC.
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T 细胞受体 (TCR) 与自肽主要组织相容性复合物 (pMHC) 的相互作用对于 T 细胞发育至关重要，但它们在外周 T 细胞反应中的作用仍不清楚。李斯特菌特异性 LLO56 和 LLO118 TCR 转基因 T 细胞的特异性和非特异性刺激引发了不同的白细胞介素 2 (IL-2) 和磷酸化 ERK 反应，其强度在胸腺中设定并在外周维持，与 TCR-self-pMHC 亲和力成比例。自身 pMHC 的撤回显着损害了 LLO56 在体内向李斯特菌的扩增。尽管它们的自身反应性明显不同，但 LLO56 和 LLO118 以相同的亲和力结合同源 pMHC，这对这些参数之间的关联提出了挑战。我们的研究结果强调了选择胸腺教育过程中遇到的配体在确定 CD4+ T 细胞的内在功能方面的关键作用。
T cell receptor (TCR) interactions with self-peptide-major histocompatibility complex (pMHC) are crucial to T cell development, but their role in peripheral T cell responses remains unclear. Specific and nonspecific stimulation of Listeria-specific LLO56 and LLO118 TCR transgenic T cells elicited distinct interleukin 2 (IL-2) and phospho-ERK responses, the strength of which was set in the thymus and maintained in the periphery in proportion to TCR-self-pMHC avidity. Withdrawal of self-pMHC markedly compromised LLO56 expansion to Listeria in vivo. Despite their markedly different self-reactivities, LLO56 and LLO118 bound cognate-pMHC with identical affinities, challenging associations made between these parameters. Our findings highlight a crucial role for selecting ligands encountered during thymic education in determining the intrinsic functionality of CD4+ T cells.
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