上海交通大学医学院张臻和张敏团队合作发现，淋巴内皮转录因子Tbx1促进免疫抑制微环境促进心肌梗死(MI)后修复。2023年8月24日，国际知名学术期刊《免疫学》发表了这一成果。

他们揭示了一种未知的由Tbx1驱动的心内免疫抑制程序，Tbx1是一种编码T-box转录因子(TF)的DiGeorge综合征基因。他们发现MI后淋巴内皮细胞(LECs)诱导了明显的淋巴血管生成和免疫调节基因表达变化。

活化的LECs穿透梗死区域，作为心肌内免疫中枢，通过趋化因子Ccl21和整合素Icam1增加耐受性树突状细胞(tDCs)和调节性T细胞(Treg)的数量，从而抑制自身反应性CD8+ T细胞的扩增，促进修复性巨噬细胞的扩增，促进心肌梗死后的修复。模仿其时机和实施可能是治疗自身免疫介导的心脏病的另一种方法。

据悉，心脏是一个容易产生自身免疫的器官。对心脏来说，控制损伤性自身免疫是避免自身免疫介导的炎症性疾病的关键。然而，对于损伤性自身免疫如何在心脏中受到限制，人们知之甚少。

附：英文原文

Title: Lymphatic endothelial transcription factor Tbx1 promotes an immunosuppressive microenvironment to facilitate post-myocardial infarction repair

Author: Wenfeng Wang, Xiao Li, Xiaoning Ding, Shanshan Xiong, Zhenlei Hu, Xuan Lu, Kan Zhang, Heng Zhang, Qianwen Hu, Kaa Seng Lai, Zhongxiang Chen, Junjie Yang, Hejie Song, Ye Wang, Lu Wei, Zeyang Xia, Bin Zhou, Yulong He, Jun Pu, Xiao Liu, Rongqin Ke, Tao Wu, Chuanxin Huang, Antonio Baldini, Min Zhang, Zhen Zhang

Issue&Volume: 2023-08-24

Abstract: The heart is an autoimmune-prone organ. It is crucial for the heart to keep injury-inducedautoimmunity in check to avoid autoimmune-mediated inflammatory disease. However,little is known about how injury-induced autoimmunity is constrained in hearts. Here,we reveal an unknown intramyocardial immunosuppressive program driven by Tbx1, a DiGeorge syndrome disease gene that encodes a T-box transcription factor (TF).We found induced profound lymphangiogenic and immunomodulatory gene expression changesin lymphatic endothelial cells (LECs) after myocardial infarction (MI). The activatedLECs penetrated the infarcted area and functioned as intramyocardial immune hubs toincrease the numbers of tolerogenic dendritic cells (tDCs) and regulatory T (Treg)cells through the chemokine Ccl21 and integrin Icam1, thereby inhibiting the expansion of autoreactive CD8+ T cells and promoting reparative macrophage expansion to facilitate post-MI repair.Mimicking its timing and implementation may be an additional approach to treatingautoimmunity-mediated cardiac diseases.

DOI: 10.1016/j.immuni.2023.07.019

Source: https://www.cell.com/immunity/fulltext/S1074-7613(23)00332-1