TCR信号体的保守发育性重新布线驱动先天样淋巴细胞的耐受性。

Amanpreet Singh Chawla, Harriet J Watt, Stefan A Schattgen, Neema Skariah, Irene Saha, Kathrynne A Warrick, Masahito Ogawa, Jessica Strid, Frederic Lamoliatte, Alastair Copland, Sara Pryde, Elena Knatko, Kasper D Rasmussen, Kazu Kikuchi, Paul G Thomas, Chandrashekar Pasare, David Bending, Mahima Swamy
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引用次数: 0

摘要

天然上皮内T淋巴细胞(T- iel)是肠道内固有的T细胞,对肠道稳态至关重要。由于胸腺激动剂的选择,这些细胞表达自身反应性T细胞抗原受体(TCRs),但它们不会引起自身免疫。肠道中天然T-IELs耐受性的机制尚不清楚。利用TCR报告小鼠模型和磷蛋白组学,我们证明了TCR信号在天然t - iel中受到内在抑制。我们发现这种抑制发生在胸腺选择后,通过改变TCR信号体成分的表达,我们将这种机制称为RePrESS (TCR信号体近端元件的重布线抑制)。RePrESS在进化上是保守的,也存在于皮肤、乳房和前列腺的自体反应性先天T细胞中。在乳糜泻中,耐受性破坏与天然T-IELs中RePrESS的缺失有关。我们的研究结果揭示了一种独特的、保守的耐受性机制,涉及TCR信号重新布线,这对理解屏障组织稳态和自身免疫性疾病具有重要意义。一句话总结:自身反应性先天样T淋巴细胞通过T细胞抗原受体信号通路的重新布线来抑制发育以维持耐受性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Conserved developmental rewiring of the TCR signalosome drives tolerance in innate-like lymphocytes.

Natural intraepithelial T lymphocytes (T-IELs) are innate-like, intestine-resident T cells essential for gut homeostasis. These cells express self-reactive T cell antigen receptors (TCRs) due to thymic agonist selection, but they do not cause autoimmunity. The mechanism underlying natural T-IELs tolerance in the gut is unclear. Using TCR reporter mouse models and phosphoproteomics, we demonstrate that TCR signaling is intrinsically suppressed in natural T-IELs. We discover that this suppression occurs post-selection in the thymus through altered expression of TCR signalosome components, a mechanism we term RePrESS (Rewiring of Proximal Elements of TCR Signalosome for Suppression). RePrESS is evolutionarily conserved and also found in autoreactive innate-like T cells from skin, breast and prostate. In coeliac disease, tolerance breakdown is associated with loss of RePrESS in natural T-IELs. Our findings reveal a distinct, conserved mechanism of tolerance involving TCR signaling rewiring, with implications for understanding barrier tissue homeostasis and autoimmune disease.

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