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首页> 外文期刊>Cellular immunology >Local synthesis of immunosuppressive glucocorticoids in the intestinal epithelium regulates anti-viral immune responses
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Local synthesis of immunosuppressive glucocorticoids in the intestinal epithelium regulates anti-viral immune responses

机译：局部合成肠上皮中免疫抑制糖皮质激素调节抗病毒免疫应答

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摘要

The nuclear receptor Small Heterodimer Partner (SHP) is a transcriptional target and inhibitor of Liver Receptor Homolog 1 (LRH-1), the transcriptional regulator of intestinal glucocorticoid (GC) synthesis. The role of SHP in the regulation of intestinal GC synthesis and its impact on T cell-mediated anti-viral immune responses in the intestinal mucosa are currently not understood. Lymphocytic choriomeningitis virus (LCMV) infection promoted intestinal GC synthesis, which was enhanced in SHP-deficient mice. Intestinal GC suppressed the expansion and altered the activation of virus-specific T cells. In contrast, deletion of LRH-1 reduced intestinal GC synthesis and accelerated the expansion of cytotoxic T cells post LCMV infection. These findings show that virus-induced intestinal GC synthesis is controlled by LRH-1 and SHP, and that local steroidogenesis contributes to the maintenance of intestinal immune homeostasis. Thus, LRH-1-regulated intestinal GC synthesis could represent an interesting therapeutic target in the treatment of inflammatory disorders.
机译：核受体小异二聚体合作伙伴（SHP）是肝受体同源物（LRH-1）的转录靶和抑制剂，肠道糖皮质激素（GC）合成的转录调节剂。 SHP在肠道GC合成调节中的作用及其对肠粘膜中T细胞介导的T细胞介导的抗病毒免疫应答的影响目前不明白。淋巴细胞核心炎病毒（LCMV）感染促进肠GC合成，其在SHP缺陷小鼠中得到增强。肠GC​​抑制了膨胀并改变了病毒特异性T细胞的激活。相比之下，LRH-1降低的肠GC合成并加速了LCMV感染后细胞毒性T细胞的膨胀。这些发现表明，病毒诱导的肠GC合成由LRH-1和SHP控制，局部类固醇发生有助于维持肠免疫稳态。因此，LRH-1调节的肠GC合成可以代表治疗炎性疾病的有趣治疗靶标。

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