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September 5, 2025Cancer Immunology Research

Tumor-derived EBI3 promotes CD8+ T cell exhaustion via STAT4-IL-10/CCL5 in gastric cancer

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Authors

YYYong-Jia YanXLXin LiuDWDaohan Wang

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Overview

Analysis reveals EBI3 significantly correlates with T cell exhaustion markers in gastric cancer, suggesting potential therapeutic targets.

Key Points

  • High EBI3 expression levels in gastric cancer correlate with increased CD8+ T cell exhaustion.
  • Mechanistically, EBI3 promotes T cell exhaustion by activating STAT4, leading to increased IL-10 and CCL5 levels.
  • Development of an anti-EBI3 heptapeptide shows promise in reversing T cell exhaustion in vitro and in vivo.
  • Research suggests targeting the EBI3-STAT4-IL10/CCL5 axis may improve immunotherapy effectiveness in gastric cancer.

Cite This Study

Yan et al. (2025) studied this question.

synapsesocial.com/papers/68c23a74b210217d64780653https://doi.org/10.1158/2326-6066.cir-24-1228
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Identification of a stromal immunosuppressive barrier orchestrated by SPP1+/C1QC+ macrophages and CD8+ exhausted T cells driving gastric cancer immunotherapy resistance2025
  2. 2The m1A-SFRP2-NFAT/TOX axis governs T cell exhaustion in gastric cancer2025
  3. 3TRIM6 ablation reverses ICB resistance in MSS gastric cancer by unleashing cGAS-STING-dependent antitumor immunity2025
  4. 4Analysis of T Cell Subsets Using Multiplex Immunohistochemistry and Clinical Outcomes of Immune Checkpoint Inhibitors in Advanced Gastric Cancer Patients2025
  5. 5ECM-Induced IL-23 Drives Immune Suppression in Breast Cancer via Regulating PD-1 on Tregs2025