Tingting Xia , Zelin Zhang , Jia Xie, Hanmei Yuan, Yayi Ren, Yue Xu, Jie Ning, Bin Li, Chao Wu
{"title":"幽门螺杆菌感染者胃粘膜CD8+TRM细胞通过CXCR5-CXCL13轴募集","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<sup>+</sup> tissue-resident memory T (CD8<sup>+</sup>T<sub>RM</sub>) cells are increased in <em>Helicobacter pylori</em> (<em>H. pylori</em>) infected subjects, but the characteristics and chemotactic mechanism of CD8<sup>+</sup>T<sub>RM</sub> cells remain unknown. We demonstrated that C-X-C chemokine receptor 5 (CXCR5) was upregulated on gastric mucosal CD8<sup>+</sup>T<sub>RM</sub> cells, and gastric CXCL13 was dominantly secreted by dendritic cells and macrophages in <em>H. pylori</em> infected subjects. Gastric mucosal CD8<sup>+</sup>T<sub>RM</sub> cells from CagA+ <em>H. pylori</em> 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<sup>+</sup>T<sub>RM</sub> cells and the expression of CXCL13 was elevated in <em>H. pylori</em> infected individuals with the development of gastric diseases. In conclusion, gastric mucosal CD8<sup>+</sup>T<sub>RM</sub> cells are increased from CagA+ <em>H. pylori</em> infected subjects and could be recruited through CXCL13-CXCR5 axis, which mainly release IFN-γ and TNF-α in <em>H. pylori</em> related immune response.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"190 ","pages":"Article 156904"},"PeriodicalIF":3.7000,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"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<sup>+</sup> tissue-resident memory T (CD8<sup>+</sup>T<sub>RM</sub>) cells are increased in <em>Helicobacter pylori</em> (<em>H. pylori</em>) infected subjects, but the characteristics and chemotactic mechanism of CD8<sup>+</sup>T<sub>RM</sub> cells remain unknown. We demonstrated that C-X-C chemokine receptor 5 (CXCR5) was upregulated on gastric mucosal CD8<sup>+</sup>T<sub>RM</sub> cells, and gastric CXCL13 was dominantly secreted by dendritic cells and macrophages in <em>H. pylori</em> infected subjects. Gastric mucosal CD8<sup>+</sup>T<sub>RM</sub> cells from CagA+ <em>H. pylori</em> 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<sup>+</sup>T<sub>RM</sub> cells and the expression of CXCL13 was elevated in <em>H. pylori</em> infected individuals with the development of gastric diseases. In conclusion, gastric mucosal CD8<sup>+</sup>T<sub>RM</sub> cells are increased from CagA+ <em>H. pylori</em> infected subjects and could be recruited through CXCL13-CXCR5 axis, which mainly release IFN-γ and TNF-α in <em>H. pylori</em> related immune response.</div></div>\",\"PeriodicalId\":297,\"journal\":{\"name\":\"Cytokine\",\"volume\":\"190 \",\"pages\":\"Article 156904\"},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2025-03-14\",\"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\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","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":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Gastric mucosal CD8+TRM cells are recruited through CXCR5-CXCL13 axis in Helicobacter pylori infected subjects
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.
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.