{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ma S"],"funding":["NIDA NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS","NINDS NIH HHS","National Institutes of Health","ORFDO NIH HHS","Leukemia and Lymphoma Society"],"pagination":["255-266"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10150872"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(2)"],"pubmed_abstract":["Despite tumor-associated macrophages (TAMs) playing a key role in shaping the tumor microenvironment (TME), the mechanisms by which TAMs influence the TME and contribute to cancer progression remain unclear. Here, we show that the N<sup>6</sup>-methyladenosine reader YTHDF2 regulates the antitumor functions of TAMs. YTHDF2 deficiency in TAMs suppressed tumor growth by reprogramming TAMs toward an antitumoral phenotype and increasing their antigen cross-presentation ability, which in turn enhanced CD8<sup>+</sup> T cell-mediated antitumor immunity. YTHDF2 deficiency facilitated the reprogramming of TAMs by targeting interferon-γ-STAT1 signaling. The expression of YTHDF2 in TAMs was regulated by interleukin-10-STAT3 signaling. Selectively targeting YTHDF2 in TAMs using a Toll-like receptor 9"],"journal":["Nature immunology"],"pubmed_title":["YTHDF2 orchestrates tumor-associated macrophage reprogramming and controls antitumor immunity through CD8<sup>+</sup> T cells."],"pmcid":["PMC10150872"],"funding_grant_id":["R01 CA266457","75N99020D00005","R01 NS106170","P01 CA163205","R01 CA265095","R35 CA210087","R21 CA223400","75N95020D00005","U19 CA264512","R01 CA247550","75N93022D00005","75N92020D00005","1364-19","R01 AI129582","75N93023D00005"],"pubmed_authors":["He C","Ma S","Bissonnette MB","Zhang J","Chen J","Sun B","Duan S","Han J","Yu J","Caligiuri MA","Barr T","Kortylewski M"],"additional_accession":[]},"is_claimable":false,"name":"YTHDF2 orchestrates tumor-associated macrophage reprogramming and controls antitumor immunity through CD8<sup>+</sup> T cells.","description":"Despite tumor-associated macrophages (TAMs) playing a key role in shaping the tumor microenvironment (TME), the mechanisms by which TAMs influence the TME and contribute to cancer progression remain unclear. Here, we show that the N<sup>6</sup>-methyladenosine reader YTHDF2 regulates the antitumor functions of TAMs. YTHDF2 deficiency in TAMs suppressed tumor growth by reprogramming TAMs toward an antitumoral phenotype and increasing their antigen cross-presentation ability, which in turn enhanced CD8<sup>+</sup> T cell-mediated antitumor immunity. YTHDF2 deficiency facilitated the reprogramming of TAMs by targeting interferon-γ-STAT1 signaling. The expression of YTHDF2 in TAMs was regulated by interleukin-10-STAT3 signaling. Selectively targeting YTHDF2 in TAMs using a Toll-like receptor 9","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-05-29T03:05:54.826Z","creation":"2025-02-19T02:39:01.688Z"},"accession":"S-EPMC10150872","cross_references":{"pubmed":["36658237"],"doi":["10.1038/s41590-022-01398-6"]}}