{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo Y"],"funding":["National Natural Science Foundation of China"],"pagination":["3229-3242"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10992087"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["72(10)"],"pubmed_abstract":["Existing immune checkpoint inhibitors focus on activating T cells and show limited effectiveness in gastric cancer (GC). SIGLEC10 is identified as a novel tumor-associated macrophage-related immune checkpoint in other cancer types. However, its immunosuppressive role and clinical significance in GC remain unclear. In this study, we find a dominant expression of SIGLEC10 on CD68<sup>+</sup> macrophages in GC. SIGLEC10 can suppress the proliferation and function of tumor-infiltrating CD8<sup>+</sup> T cells in vitro via the Akt/P38/Erk signaling pathway. Furthermore, in ex vivo and in vivo models, SIGLEC10 blockade promotes CD8<sup>+</sup> T cell effector function. Finally, SIGLEC10<sup>+</sup> macrophages are positively correlated with the adverse prognosis of GC. Our study highlights that "],"journal":["Cancer immunology, immunotherapy : CII"],"pubmed_title":["SIGLEC10<sup>+</sup> macrophages drive gastric cancer progression by suppressing CD8<sup>+</sup> T cell function."],"pmcid":["PMC10992087"],"funding_grant_id":["32070878","81970497"],"pubmed_authors":["Liu X","Xie F","Guo Y","Chen J","Lu H","Xu D","Zhao G","Zhao W","Shen Y","Wang Z","Ke S"],"additional_accession":[]},"is_claimable":false,"name":"SIGLEC10<sup>+</sup> macrophages drive gastric cancer progression by suppressing CD8<sup>+</sup> T cell function.","description":"Existing immune checkpoint inhibitors focus on activating T cells and show limited effectiveness in gastric cancer (GC). SIGLEC10 is identified as a novel tumor-associated macrophage-related immune checkpoint in other cancer types. However, its immunosuppressive role and clinical significance in GC remain unclear. In this study, we find a dominant expression of SIGLEC10 on CD68<sup>+</sup> macrophages in GC. SIGLEC10 can suppress the proliferation and function of tumor-infiltrating CD8<sup>+</sup> T cells in vitro via the Akt/P38/Erk signaling pathway. Furthermore, in ex vivo and in vivo models, SIGLEC10 blockade promotes CD8<sup>+</sup> T cell effector function. Finally, SIGLEC10<sup>+</sup> macrophages are positively correlated with the adverse prognosis of GC. Our study highlights that ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Oct","modification":"2026-04-29T14:06:52.418Z","creation":"2026-04-07T15:15:16.799Z"},"accession":"S-EPMC10992087","cross_references":{"pubmed":["37432407"],"doi":["10.1007/s00262-023-03488-2"]}}