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科学家发现CD97通过红细胞的机械感应促进脾脏树突状细胞的稳态
作者:小柯机器人 发布时间:2022/2/13 21:39:34

美国加州大学Jason G. Cyster团队近期取得新的研究进展,他们发现CD97通过红细胞的机械感应促进脾脏树突状细胞的稳态。该项成果于2022年2月11日出版在《科学》杂志上。

研究人员发现,脾脏中的2型常规DCs(cDC2s)依赖于Gα13和粘附G蛋白偶联受体家族成员-E5 (Adgre5或CD97)定位于血液暴露的位置。CD97功能活性需要其自身蛋白水解切割激活。 CD55是CD97的配体,在剪切应力条件下,cDC2与表达CD55的红细胞(RBC)相互作用导致调节性CD97 N端片段的提取。CD55-CD97信号传导的缺陷导致脾脏cDC2丢失进入循环和淋巴细胞对血源性抗原的反应缺陷。 因此,红细胞的CD97机械感应建立了一个迁移和基因表达程序,优化了脾cDC2的抗原捕获和呈递功能。

据介绍,树突状细胞 (DC) 对于启动适应性免疫反应至关重要。 然而,控制DC定位和稳态的因素尚不完全清楚。

附:英文原文

Title: CD97 promotes spleen dendritic cell homeostasis through the mechanosensing of red blood cells

Author: Dan Liu, Lihui Duan, Lauren B. Rodda, Erick Lu, Ying Xu, Jinping An, Longhui Qiu, Fengchun Liu, Mark R. Looney, Zhiyong Yang, Christopher D. C. Allen, Zhongmei Li, Alexander Marson, Jason G. Cyster

Issue&Volume: 2022-02-11

Abstract: Dendritic cells (DCs) are crucial for initiating adaptive immune responses. However, the factors that control DC positioning and homeostasis are incompletely understood. We found that type-2 conventional DCs (cDC2s) in the spleen depend on Gα13 and adhesion G protein-coupled receptor family member-E5 (Adgre5, or CD97) for positioning in blood-exposed locations. CD97 function required its autoproteolytic cleavage. CD55 is a CD97 ligand, and cDC2 interaction with CD55-expressing red blood cells (RBCs) under shear stress conditions caused extraction of the regulatory CD97 N-terminal fragment. Deficiency in CD55-CD97 signaling led to loss of splenic cDC2s into the circulation and defective lymphocyte responses to blood-borne antigens. Thus, CD97 mechanosensing of RBCs establishes a migration and gene expression program that optimizes the antigen capture and presentation functions of splenic cDC2s.

DOI: abi5965

Source: https://www.science.org/doi/10.1126/science.abi5965

 

期刊信息
Science:《科学》,创刊于1880年。隶属于美国科学促进会,最新IF:41.037