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C/EBPδ 驱动人类 MAIT 细胞与内皮细胞之间的相互作用，这对于血管外渗是很重要的。

C/EBPδ drives interactions between human MAIT cells and endothelial cells that are important for extravasation.

机构信息

Inflammation Biology Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.

Biological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.

出版信息

Elife. 2018 Feb 22;7:e32532. doi: 10.7554/eLife.32532.

DOI:10.7554/eLife.32532
PMID:29469805
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5869018/
Abstract

Many mediators and regulators of extravasation by bona fide human memory-phenotype T cells remain undefined. Mucosal-associated invariant T (MAIT) cells are innate-like, antibacterial cells that we found excelled at crossing inflamed endothelium. They displayed abundant selectin ligands, with high expression of and , and expressed CCR6, CCR5, and CCR2, which played non-redundant roles in trafficking on activated endothelial cells. MAIT cells selectively expressed CCAAT/enhancer-binding protein delta (C/EBPδ). Knockdown of C/EBPδ diminished expression of , and decreasing MAIT cell rolling and arrest, and consequently the cells' ability to cross an endothelial monolayer in vitro and extravasate in mice. Nonetheless, knockdown of C/EBPδ did not affect , which was important for the step of transendothelial migration. Thus, MAIT cells demonstrate a program for extravasastion that includes, in part, C/EBPδ and C/EBPδ-regulated genes, and that could be used to enhance, or targeted to inhibit T cell recruitment into inflamed tissue.

摘要

许多真正的人类记忆表型 T 细胞外渗的介质和调节剂仍未被定义。黏膜相关不变 T（MAIT）细胞是先天样的抗细菌细胞，我们发现它们擅长穿过发炎的内皮细胞。它们表现出丰富的选择素配体，高表达 和 ，并表达 CCR6、CCR5 和 CCR2，它们在激活的内皮细胞上的迁移中发挥非冗余作用。MAIT 细胞选择性表达 CCAAT/增强子结合蛋白 delta（C/EBPδ）。C/EBPδ 的敲低降低了 和 的表达，减少了 MAIT 细胞的滚动和附着，从而降低了细胞在体外穿过内皮单层和在小鼠中渗出的能力。尽管如此，C/EBPδ 的敲低并不影响 ，这对于跨内皮迁移步骤很重要。因此，MAIT 细胞表现出一种外渗程序，其中部分包括 C/EBPδ 和 C/EBPδ 调节的基因，这可以用于增强或靶向抑制 T 细胞募集到炎症组织中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d250/5869018/b1e6439aaec4/elife-32532-fig7-figsupp2.jpg
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