Thymocytes that bind with high affinity to peptides displayed by MHC class II (pMHC‐II) are deleted while low‐affinity binders differentiate into naive CD4+ T cells. However, Foxp3+ regulatory T cells (Tregs) seem to defy this binary choice as their precursors require high‐affinity interaction with pMHC‐II for maturation in the thymus. Here, we rely on the antigen‐specific interpretive framework, SPIRAL (Specific ImmunoRegulatory Algorithm), to propose that Tregs escape thymic deletion by forming dyads with IL‐2‐producing T cells via antigen cross‐reactivity. This interpretation reconciles contradictions related to Treg ontogeny in the thymus and their role in modulating antigen‐specific immune responses.

中文翻译：

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交叉反应能否从胸腺缺失中拯救Foxp3 +调节性T细胞前体？

与II类MHC（pMHC-II）展示的肽具有高亲和力的胸腺细胞被删除，而低亲和力的结合物则分化为幼稚的CD4 + T细胞。但是，Foxp3 +调节性T细胞（Tregs）似乎无视这种二元选择，因为它们的前体需要与pMHC-II高亲和力相互作用才能在胸腺中成熟。在这里，我们依靠抗原特异性解释性框架，螺旋（SP ecific我mmuno ř egulatory铝gorithm），提议的Treg通过经由抗原交叉反应的IL-2的T细胞形成成对层逸出胸腺缺失。这种解释调和了与胸腺中Treg个体发育有关的矛盾及其在调节抗原特异性免疫反应中的作用。