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首页> 外文期刊>The Journal of investigative dermatology. >Selective upregulation of fibroblast Fas ligand expression, and prolongation of Fas/Fas ligand-mediated skin allograft survival, by retinoic acid: the skin as a retinoide-inducible immune privilege site.
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Selective upregulation of fibroblast Fas ligand expression, and prolongation of Fas/Fas ligand-mediated skin allograft survival, by retinoic acid: the skin as a retinoide-inducible immune privilege site.

机译：维甲酸可选择性上调成纤维细胞Fas配体的表达，并延长Fas / Fas配体介导的皮肤同种异体移植物的存活：作为维甲酸诱导的免疫特权位点的皮肤。

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摘要

Fas/Fas ligand-mediated lymphocyte apoptosis has been implicated in the suppression of immune responses and may cause immune privilege. Human corneas exhibit immune privilege and can be transplanted across allogeneic barriers without immunosuppressive therapy, perhaps, because corneal keratinocytes express Fas ligand. To characterize Fas and Fas ligand expression in skin, we examined expression by murine keratinocytes, dermal fibroblasts, melanocytes, and human umbilical endothelial cells. We also studied the regulation of Fas and Fas ligand in skin cells by retinoic acid, vitamin D3, and dexamethasone as well as various cytokines. Among the molecules and cells tested, retinoic acid selectively upregulated the expression of Fas ligand molecule by fibroblasts. Retinoic acid-induced Fas ligand+ fibroblasts killed Fas+ target cells, and this killing was blocked by anti-Fas ligand antibody. The function of Fas ligand on dermal fibroblasts in vivo was tested in a cutaneous allograft system. Histoincompatible BALB/C mouse (H-2d) donor skin was grafted on to allogeneic C57BL/6 mice (H-2b). Daily local injection of retinoic acid blocked inflammation and extended graft survival for more than 10 d. Injection of retinoic acid into Fas ligand mutated gld/gld donor skin did not prevent leukocyte infiltration into the allograft or prolong graft survival. These experiments indicate that, in skin, retinoic acid selectively increases Fas ligand expression by fibroblasts and that retinoic acid has potent Fas/Fas ligand-dependent immunosuppressive activity.
机译：Fas / Fas配体介导的淋巴细胞凋亡与免疫应答的抑制有关，并可能导致免疫特权。人类角膜具有免疫特权，无需免疫抑制疗法即可跨异体屏障移植，这可能是因为角膜角质形成细胞表达Fas配体。为了表征Fas和Fas配体在皮肤中的表达，我们检查了鼠角质形成细胞，真皮成纤维细胞，黑素细胞和人脐带内皮细胞的表达。我们还研究了视黄酸，维生素D3和地塞米松以及多种细胞因子对皮肤细胞中Fas和Fas配体的调节作用。在测试的分子和细胞中，视黄酸通过成纤维细胞选择性上调了Fas配体分子的表达。维甲酸诱导的Fas配体+成纤维细胞杀死了Fas +靶细胞，这种杀死被抗Fas配体抗体阻断。在皮肤同种异体移植系统中测试了Fas配体在体内真皮成纤维细胞上的功能。将组织相容性BALB / C小鼠（H-2d）供体皮肤移植到同种异体C57BL / 6小鼠（H-2b）上。每天局部注射视黄酸可阻止炎症，并使移植物存活时间延长10天以上。向Fas配体突变的gld / gld供体皮肤中注射视黄酸并不能阻止白细胞浸入同种异体移植物中或延长移植物的存活时间。这些实验表明，在皮肤中，视黄酸通过成纤维细胞选择性地增加Fas配体的表达，并且视黄酸具有有效的Fas / Fas配体依赖性免疫抑制活性。

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