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A 'hotspot' for autoimmune T cells in type 1 diabetes

机译:1型糖尿病自身免疫性T细胞的“热点”

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摘要

The ability of a single T cell antigen receptor (TCR) to cross-react with multiple antigens allows the finite number of T cells within an organism to respond to the compendium of pathogen challenges faced during a lifetime. Effective immune surveillance, however, comes at a price. TCR cross-reactivity can allow molecular mimics to spuriously activate autoimmune T cells; it also underlies T cell rejection of organ transplants and drives graft-versus-host disease. In this issue of the JCI, Cole and colleagues provide insight into how an insulin-reactive T cell cross-reacts with pathogen-derived antigens by focusing on a limited portion of the peptides to provide a hotspot for binding. These findings dovetail with recent studies of alloreactive and autoimmune TCRs and suggest that the biochemical principles that govern conventional protein-protein interactions may allow the specificity and cross-reactivity profiles of T cells to be predicted.
机译:单个 T 细胞抗原受体 (TCR) 与多种抗原发生交叉反应的能力使生物体内有限数量的 T 细胞能够应对一生中面临的病原体挑战纲要。然而,有效的免疫监测是有代价的。TCR 交叉反应性可使分子模拟物虚假地激活自身免疫性 T 细胞;它也是器官移植 T 细胞排斥反应的基础,并导致移植物抗宿主病。在本期JCI中,Cole及其同事通过关注肽的有限部分来提供结合热点,从而深入了解胰岛素反应性T细胞如何与病原体衍生的抗原发生交叉反应。这些发现与最近对同种异体反应性和自身免疫性TCR的研究相吻合,并表明控制传统蛋白质-蛋白质相互作用的生化原理可能允许预测T细胞的特异性和交叉反应性特征。

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