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

  • Cytokine. 2025 Mar 14:190:156904. doi: 10.1016/j.cyto.2025.156904.
Tingting Xia  1 ,  Zelin Zhang  1 ,  Jia Xie  1 ,  Hanmei Yuan  1 ,  Yayi Ren  1 ,  Yue Xu  1 ,  Jie Ning  1 ,  Bin Li  1 ,  Chao Wu  2
Affiliations
  • 1. Department of Laboratory Medicine, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
  • 2. Department of Laboratory Medicine, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, China. Electronic address: [email protected].
PMID: 40088523 DOI: 10.1016/j.cyto.2025.156904
Abstract

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.

Keywords
CD8(+) tissue-resident memory T cells; Cell chemotaxis; Cytotoxin-associated gene a; Gastric mucosa; Helicobacter pylori.
Products