2. Academic Validation
  3. Gastric mucosal CD8+TRM cells are recruited through CXCR5-CXCL13 axis in Helicobacter pylori infected subjects

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

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: chaowu261@163.com.
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.

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