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首页> 外文期刊>The Journal of investigative dermatology. >UVR-induced regulatory T cells switch antigen-presenting cells from a stimulatory to a regulatory phenotype.
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UVR-induced regulatory T cells switch antigen-presenting cells from a stimulatory to a regulatory phenotype.

机译：UVR诱导的调节性T细胞将抗原呈递细胞从刺激性表型转换为调节性表型。

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UVR-induced regulatory T cells (UVR-Treg) inhibit sensitization in an antigen-specific manner. The migratory behavior of UVR-Treg can be reprogrammed by antigen-presenting cells (APCs), indicating a cross-talk between these cells. Hence, we sought to investigate whether in turn UVR-Treg can influence APCs. Bone marrow-derived dendritic cells (DCs) were co-incubated with DNFB-specific UVR-Treg. DCs were isolated, coupled with DNBS, and injected into naive mice. Contrary to untreated dinitrobenzenesulfonic acid (DNBS)-coupled DC, DCs from the cocultures failed to induce sensitization in the recipients. Antibody blocking and transwell experiments indicated that both IL-10 and cellular contact are required during the co-incubation to induce inhibition. UVR-Treg downregulated B7-2 and major histocompatibility complex class II but induced the negative regulatory molecules B7-H3 and B7-H4 on DC. To suppress, UVR-Treg had to be activated in an antigen-specific manner. However, the suppression was not antigen-specific as activated DNFB-specific UVR-Treg inhibited DCs to sensitize also against trinitrochlorobenzene. Adoptive transfer experiments revealed that injection of hapten-coupled DCs, which were co-incubated with UVR-Treg, further induced Treg in the recipients. Together, this indicates that activated UVR-Treg can alter APCs in such a way that they lose their sensitizing capacity but in turn induce Treg. Thus, UVR-Tregs switch APCs from a stimulatory to a regulatory phenotype.
机译：UVR诱导的调节性T细胞（UVR-Treg）以抗原特异性方式抑制致敏作用。可以通过抗原呈递细胞（APC）对UVR-Treg的迁移行为进行重新编程，表明这些细胞之间存在串扰。因此，我们试图研究UVR-Treg是否会影响APC。将骨髓来源的树突状细胞（DC）与DNFB特异性UVR-Treg共孵育。分离DC，与DNBS偶联，并注射到幼稚小鼠中。与未经处理的二硝基苯磺酸（DNBS）偶联的DC相反，来自共培养物的DC无法在受体中诱导致敏。抗体阻断和穿孔实验表明，在共孵育过程中需要IL-10和细胞接触才能诱导抑制作用。 UVR-Treg下调B7-2和II类主要组织相容性复合物，但在DC上诱导了负调控分子B7-H3和B7-H4。为了抑制，必须以抗原特异性方式激活UVR-Treg。但是，该抑制不是抗原特异性的，因为活化的DNFB特异性UVR-Treg抑制了DC对三硝基氯苯也敏感。过继转移实验表明，与UVR-Treg共孵育的半抗原偶联DC的注射进一步在受体中诱导了Treg。总之，这表明活化的UVR-Treg可以改变APC，使其失去敏化能力，但又诱导Treg。因此，UVR-Tregs将APC从刺激表型转换为调节表型。

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