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免疫检查点分子:皮肤光免疫学领域的“新”成员。

Immune checkpoint molecules: "new" kids on the block of skin photoimmunology.

作者信息

Wang Wei, Wu Zhao-Hui

机构信息

Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN, USA.

Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.

出版信息

Genes Dis. 2019 Dec 4;8(1):1-5. doi: 10.1016/j.gendis.2019.11.002. eCollection 2021 Jan.

DOI:10.1016/j.gendis.2019.11.002
PMID:33569508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7859459/
Abstract

Ultraviolet radiation (UVR) is a prominent etiological factor of the pathogenesis of skin diseases such as squamous cell carcinoma and melanoma. Excessive exposure to the natural sources of UVR such as sunlight or artificially from tanning lamps has been linked to the increasing incidence of skin cancers in the United States. Besides the skin inflammation, DNA damage and oncogenic mutation caused by UVR, UV exposure also plays a critical role in suppressing local and systemic immune responses which enable premalignant and cancer cells to escape immune surveillance. A variety of mechanisms have been reported to regulate the immune-suppressive effects of UVR. Here we discuss the current understanding of how UV modulates the local and systemic immunity, the recent progress in roles of immune checkpoint molecules in UVR-induced immune suppression, and how the crosstalk between the immune cells may shape the immune landscape of the skin upon UVR.

摘要

紫外线辐射(UVR)是鳞状细胞癌和黑色素瘤等皮肤病发病机制中的一个重要病因。过度暴露于UVR的自然来源(如阳光)或人工来源(如晒黑灯)与美国皮肤癌发病率的上升有关。除了UVR引起的皮肤炎症、DNA损伤和致癌突变外,紫外线暴露在抑制局部和全身免疫反应中也起着关键作用,这使得癌前细胞和癌细胞能够逃避免疫监视。据报道,有多种机制可调节UVR的免疫抑制作用。在此,我们讨论目前对紫外线如何调节局部和全身免疫的理解、免疫检查点分子在UVR诱导的免疫抑制中的作用的最新进展,以及免疫细胞之间的相互作用如何塑造紫外线照射后皮肤的免疫格局。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe6b/7859459/034a7d61a65f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe6b/7859459/034a7d61a65f/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe6b/7859459/034a7d61a65f/gr1.jpg

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本文引用的文献

1
Upregulation of PD-L1 via HMGB1-Activated IRF3 and NF-κB Contributes to UV Radiation-Induced Immune Suppression.高迁移率族蛋白 B1 通过激活干扰素调节因子 3 和核因子 κB 上调 PD-L1,导致紫外线辐射诱导的免疫抑制。
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