{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["De Simone G"],"funding":["European Research Council"],"pagination":["2089-2100.e8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8459394"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["54(9)"],"pubmed_abstract":["Kupffer cells (KCs) are highly abundant, intravascular, liver-resident macrophages known for their scavenger and phagocytic functions. KCs can also present antigens to CD8<sup>+</sup> T cells and promote either tolerance or effector differentiation, but the mechanisms underlying these discrepant outcomes are poorly understood. Here, we used a mouse model of hepatitis B virus (HBV) infection, in which HBV-specific naive CD8<sup>+</sup> T cells recognizing hepatocellular antigens are driven into a state of immune dysfunction, to identify a subset of KCs (referred to as KC2) that cross-presents hepatocellular antigens upon interleukin-2 (IL-2) administration, thus improving the antiviral function of T cells. Removing MHC-I from all KCs, including KC2, or selectively depleting KC2 impaired the"],"journal":["Immunity"],"pubmed_title":["Identification of a Kupffer cell subset capable of reverting the T cell dysfunction induced by hepatocellular priming."],"pmcid":["PMC8459394"],"funding_grant_id":["957502","725038"],"pubmed_authors":["Garcia-Manteiga JM","Ficht X","Andreata F","Guidotti LG","Bleriot C","Gilotto S","Moalli F","Bono EB","Chakarov S","Mainetti M","Ambrosi G","Giustini L","Zordan P","Benechet AP","Ginhoux F","De Simone G","Iannacone M","Laura C","Bajenoff M","Fumagalli V","Di Lucia P","De Ponti FF","Rava M"],"additional_accession":[]},"is_claimable":false,"name":"Identification of a Kupffer cell subset capable of reverting the T cell dysfunction induced by hepatocellular priming.","description":"Kupffer cells (KCs) are highly abundant, intravascular, liver-resident macrophages known for their scavenger and phagocytic functions. KCs can also present antigens to CD8<sup>+</sup> T cells and promote either tolerance or effector differentiation, but the mechanisms underlying these discrepant outcomes are poorly understood. Here, we used a mouse model of hepatitis B virus (HBV) infection, in which HBV-specific naive CD8<sup>+</sup> T cells recognizing hepatocellular antigens are driven into a state of immune dysfunction, to identify a subset of KCs (referred to as KC2) that cross-presents hepatocellular antigens upon interleukin-2 (IL-2) administration, thus improving the antiviral function of T cells. Removing MHC-I from all KCs, including KC2, or selectively depleting KC2 impaired the","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-06-17T05:14:39.127Z","creation":"2022-02-11T11:29:29.957Z"},"accession":"S-EPMC8459394","cross_references":{"pubmed":["34469774"],"doi":["10.1016/j.immuni.2021.05.005"]}}