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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Thrombospondin-1-dependent immune regulation by transforming growth factor-beta(2)-exposed antigen-presenting cells
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Thrombospondin-1-dependent immune regulation by transforming growth factor-beta(2)-exposed antigen-presenting cells

机译：通过转化生长因子-β（2）-暴露的抗原呈递细胞的血小板反应蛋白-1依赖性免疫调节。

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An important role of transforming growth factor-beta (TGF-beta) in the development of regulatory T cells is well established. Although integrin-mediated activation of latent TGF-beta(1) is considered essential for the induction of regulatory T (Treg) cells by antigen-presenting cells (APCs), such an activation mechanism is not applicable to the TGF-beta(2) isoform, which lacks an integrin-binding RGD sequence in its latency-associated peptide. Mucosal and ocular tissues harbour TGF-beta(2)-expressing APCs involved in Treg induction. The mechanisms that regulate TGF-beta activation in such APCs remain unclear. In this study, we demonstrate that murine APCs exposed to TGF-beta(2) in the environment predominantly increase expression of TGF-beta(2). Such predominantly TGF-beta(2)-expressing APCs use thrombospondin- 1 (TSP-1) as an integrin-independent mechanism to activate their newly synthesized latent TGF-beta(2) to induce Foxp3(+) Treg cells both in vitro and in vivo. Expression of Treg induction by TGF-beta(2)-expressing APCs is supported by a TSP-1 receptor, CD36, which facilitates activation of latent TGF-beta during antigen presentation. Our results suggest that APC-derived TSP-1 is essential for the development of an adaptive regulatory immune response induced by TGF-beta(2)-expressing APCs similar to those located at mucosal and ocular sites. These findings introduce the integrin-independent mechanism of TGF-beta activation as an integral part of peripheral immune tolerance associated with TGF-beta(2)-expressing tissues.
机译：众所周知，在调节性T细胞的发育中，转化生长因子-β（TGF-beta）的重要作用。尽管整联蛋白介导的潜在TGF-beta（1）激活被认为是抗原呈递细胞（APC）诱导调节性T（Treg）细胞所必需的，但这种激活机制不适用于TGF-beta（2）异构体，在其潜伏期相关肽中缺少整合素结合的RGD序列。粘膜和眼组织具有参与Treg诱导的表达TGF-beta（2）的APC。在这种APC中调节TGF-β激活的机制仍不清楚。在这项研究中，我们证明暴露在环境中的TGF-beta（2）的鼠APC主要增加TGF-beta（2）的表达。此类主要表达TGF-β（2）的APC使用血小板反应蛋白1（TSP-1）作为整联蛋白非依赖性机制来激活其新合成的潜在TGF-β（2），以在体外和体外诱导Foxp3（+）Treg细胞。体内。 TSP-β（2）表达的APC对Treg诱导的表达受TSP-1受体CD36的支持，CD36有助于在抗原呈递过程中激活潜在的TGF-β。我们的结果表明，APC衍生的TSP-1对于由TGF-beta（2）表达的APC诱导的适应性调节免疫应答的发展至关重要，该APC与位于粘膜和眼部的类似。这些发现介绍了TGF-β激活的整合素独立机制，作为与表达TGF-β（2）的组织相关的外周免疫耐受的组成部分。

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