Gastric mucosal CD8+TRM cells are recruited through CXCR5-CXCL13 axis in Helicobacter pylori infected subjects

IF 3.7 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Cytokine Pub Date : 2025-06-01 Epub Date: 2025-03-14 DOI:10.1016/j.cyto.2025.156904

Tingting Xia , Zelin Zhang , Jia Xie, Hanmei Yuan, Yayi Ren, Yue Xu, Jie Ning, Bin Li, Chao Wu

{"title":"Gastric mucosal CD8+TRM cells are recruited through CXCR5-CXCL13 axis in Helicobacter pylori infected subjects","authors":"Tingting Xia , Zelin Zhang , Jia Xie, Hanmei Yuan, Yayi Ren, Yue Xu, Jie Ning, Bin Li, Chao Wu","doi":"10.1016/j.cyto.2025.156904","DOIUrl":null,"url":null,"abstract":"<div><div>Gastric mucosal CD8+ tissue-resident memory T (CD8+TRM) cells are increased in Helicobacter pylori (H. pylori) infected subjects, but the characteristics and chemotactic mechanism of CD8+TRM cells remain unknown. We demonstrated that C-X-C chemokine receptor 5 (CXCR5) was upregulated on gastric mucosal CD8+TRM cells, and gastric CXCL13 was dominantly secreted by dendritic cells and macrophages in H. pylori infected subjects. Gastric mucosal CD8+TRM cells from CagA+ H. pylori infected subjects was increased and could secrete more IFN-γ and TNF-α to engage in local immune response. The number of gastric mucosal CD8+TRM cells and the expression of CXCL13 was elevated in H. pylori infected individuals with the development of gastric diseases. In conclusion, gastric mucosal CD8+TRM cells are increased from CagA+ H. pylori infected subjects and could be recruited through CXCL13-CXCR5 axis, which mainly release IFN-γ and TNF-α in H. pylori related immune response.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156904"},"PeriodicalIF":3.7000,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytokine","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1043466625000511","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/14 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Gastric mucosal CD8⁺ tissue-resident memory T (CD8⁺T_RM) cells are increased in Helicobacter pylori (H. pylori) infected subjects, but the characteristics and chemotactic mechanism of CD8⁺T_RM cells remain unknown. We demonstrated that C-X-C chemokine receptor 5 (CXCR5) was upregulated on gastric mucosal CD8⁺T_RM cells, and gastric CXCL13 was dominantly secreted by dendritic cells and macrophages in H. pylori infected subjects. Gastric mucosal CD8⁺T_RM cells from CagA+ H. pylori infected subjects was increased and could secrete more IFN-γ and TNF-α to engage in local immune response. The number of gastric mucosal CD8⁺T_RM cells and the expression of CXCL13 was elevated in H. pylori infected individuals with the development of gastric diseases. In conclusion, gastric mucosal CD8⁺T_RM cells are increased from CagA+ H. pylori infected subjects and could be recruited through CXCL13-CXCR5 axis, which mainly release IFN-γ and TNF-α in H. pylori related immune response.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

幽门螺杆菌感染者胃粘膜CD8+TRM细胞通过CXCR5-CXCL13轴募集

幽门螺杆菌感染患者胃粘膜CD8+组织常驻记忆T （CD8+TRM）细胞增多，但CD8+TRM细胞的特征和趋化机制尚不清楚。我们发现C-X-C趋化因子受体5 （CXCR5）在胃粘膜CD8+TRM细胞中上调，而胃CXCL13主要由幽门螺杆菌感染的树突状细胞和巨噬细胞分泌。CagA+幽门螺杆菌感染患者胃黏膜CD8+TRM细胞增多，可分泌更多IFN-γ和TNF-α参与局部免疫应答。随着胃疾病的发展，幽门螺杆菌感染个体胃黏膜CD8+TRM细胞数量和CXCL13表达升高。综上所示，CagA+幽门螺杆菌感染患者胃粘膜CD8+TRM细胞增加，可通过CXCL13-CXCR5轴募集，在幽门螺杆菌相关免疫应答中主要释放IFN-γ和TNF-α。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

文献相关原料

公司名称

产品信息

索莱宝

EDTA

索莱宝

DAPI

来源期刊

Cytokine 医学-免疫学

CiteScore

7.60

自引率

2.60%

发文量

262

审稿时长

48 days

期刊介绍： The journal Cytokine has an open access mirror journal Cytokine: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. * Devoted exclusively to the study of the molecular biology, genetics, biochemistry, immunology, genome-wide association studies, pathobiology, diagnostic and clinical applications of all known interleukins, hematopoietic factors, growth factors, cytotoxins, interferons, new cytokines, and chemokines, Cytokine provides comprehensive coverage of cytokines and their mechanisms of actions, 12 times a year by publishing original high quality refereed scientific papers from prominent investigators in both the academic and industrial sectors. We will publish 3 major types of manuscripts: 1) Original manuscripts describing research results. 2) Basic and clinical reviews describing cytokine actions and regulation. 3) Short commentaries/perspectives on recently published aspects of cytokines, pathogenesis and clinical results.