{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zeituni-Timor O"],"funding":["Rosetrees Trust","Wolfson Family Charitable Trust","Israel Science Foundation","Israel Science Foundation (ISF)","Wolfson Family Charitable Trust (WFCT)"],"pagination":["1269"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12375040"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["During the resolution of inflammation, Ly6C+F4/80- monocytes differentiate to Ly6C-F4/80+ macrophages that exert apoptotic cell engulfment (efferocytosis) properties and consequently convert to interferon (IFN)-β-producing macrophages. Here, we report that exposure to IFN-β, or transforming growth factor (TGF)-β, or a deficiency in the pro-apoptotic protein ARTS, results in the conversion of mature macrophages to an Ly6C+F4/80+CCR2+ phenotype in vivo and ex vivo. Deficiency in ARTS or caspase inhibition results in enhanced conversion of macrophages to the Ly6C+ phenotype. Moreover, IFN-β-triggered Ly6C+ macrophages are hyper-efferocytic and express higher levels of the efferocytic receptor CD36. Inhibition of CD36 ligation results in complete abrogation of efferocytosis ex vivo in both Ly6"],"journal":["Communications biology"],"pubmed_title":["IFN-β and ARTS deficiency promote the generation of hyper-efferocytic Ly6C<sup>+</sup> macrophages in resolving inflammation in male mice."],"pmcid":["PMC12375040"],"funding_grant_id":["NA","678/13"],"pubmed_authors":["Zeituni-Timor O","Kumaran Satyanarayanan S","Abu Zeid M","Ariel A","Goswami P","Silberberg E","Larisch S","Soboh S","Yaseen H","Schif-Zuck S","Zaid A"],"additional_accession":[]},"is_claimable":false,"name":"IFN-β and ARTS deficiency promote the generation of hyper-efferocytic Ly6C<sup>+</sup> macrophages in resolving inflammation in male mice.","description":"During the resolution of inflammation, Ly6C+F4/80- monocytes differentiate to Ly6C-F4/80+ macrophages that exert apoptotic cell engulfment (efferocytosis) properties and consequently convert to interferon (IFN)-β-producing macrophages. Here, we report that exposure to IFN-β, or transforming growth factor (TGF)-β, or a deficiency in the pro-apoptotic protein ARTS, results in the conversion of mature macrophages to an Ly6C+F4/80+CCR2+ phenotype in vivo and ex vivo. Deficiency in ARTS or caspase inhibition results in enhanced conversion of macrophages to the Ly6C+ phenotype. Moreover, IFN-β-triggered Ly6C+ macrophages are hyper-efferocytic and express higher levels of the efferocytic receptor CD36. Inhibition of CD36 ligation results in complete abrogation of efferocytosis ex vivo in both Ly6","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-05-09T10:33:37.117Z","creation":"2026-04-08T00:46:45.248Z"},"accession":"S-EPMC12375040","cross_references":{"pubmed":["40849518"],"doi":["10.1038/s42003-025-08707-3"]}}