当前位置:科学网首页 > 小柯机器人 >详情
巨噬细胞MR1抗原呈递促进MAIT细胞免疫和肺微生物群调节
作者:小柯机器人 发布时间:2025/12/5 17:36:23

墨尔本大学Hamish E. G. McWilliam团队的最新研究提出了巨噬细胞MR1抗原呈递促进MAIT细胞免疫和肺微生物群调节。这一研究成果于2025年12月4日发表在国际顶尖学术期刊《科学》上。

该课题组发现MR1的表达在不同的组织和细胞类型中是不同的。来自肺和腹腔的巨噬细胞表达最高水平的MR1,并且最有效地捕获VitBAg并将其呈递给MAIT细胞。巨噬细胞中MR1的表达受组织环境和微生物群的转录调控和诱导。巨噬细胞、树突状细胞和单核细胞中MR1的缺失改变了微生物群的组成,削弱了MAIT细胞对细菌感染的反应。该课题组得出结论,巨噬细胞是MR1抗原呈递和MAIT细胞免疫的关键。

据悉,粘膜相关不变性T (MAIT)细胞介导组织稳态和抗菌免疫。然而,表达MHC I类相关蛋白1 (MR1)并向MAIT细胞呈递微生物维生素B衍生抗原(VitBAg)的细胞尚不清楚。

附:英文原文

Title: Macrophage MR1 antigen presentation promotes MAIT cell immunity and lung microbiota modulation

Author: Jieru Deng, Yuting Yan, Xiaoyue Zhang, Calum J. Walsh, Emmanuel Montassier, Debajyoti Sinha, Huimeng Wang, Atieh Mousavizadeh, Mitra Ashayeripanah, Jeffrey Y. W. Mak, Hui-Fern Koay, Tobias Poch, Yannick O. Alexandre, Scott N. Mueller, Ajithkumar Vasanthakumar, Tim P. Stinear, Vanta J. Jameson, Alexis Perez-Gonzalez, Jenny Kingham, Tri Giang Phan, Nikita Potemkin, Lachlan Dryburgh, Jan Schroeder, David P. Fairlie, Laura K. Mackay, Zhenjun Chen, Laura Cook, Abderrahman Hachani, Alexandra J. Corbett, Antoine Roquilly, Jose A. Villadangos, Hamish E. G. McWilliam

Issue&Volume: 2025-12-04

Abstract: Mucosal associated invariant T (MAIT) cells mediate tissue homeostasis and antimicrobial immunity. However, the cells that express MHC class I-related protein 1 (MR1) and present microbial vitamin B-derived antigens (VitBAg) to MAIT cells remain unknown. We found that MR1 expression varied across tissues and cell types. Macrophages from the lung and peritoneal cavity expressed the highest levels of MR1 and were the most efficient at capturing and presenting VitBAg to MAIT cells. Expression of MR1 in macrophages was regulated transcriptionally and induced by the tissue environment and microbiota. Depletion of MR1 in macrophages, dendritic cells and monocytes changed the composition of the microbiota and impaired MAIT cell responses against bacterial infection. We concluded that macrophages are key for MR1 antigen presentation and MAIT cell immunity.

DOI: adr6322

Source: https://www.science.org/doi/10.1126/science.adr6322

 

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:63.714