{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Barlev AN"],"funding":["NIAID NIH HHS","American Autoimmune Related Disease Association","National Institutes of Health"],"pagination":["e157250"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9435648"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(17)"],"pubmed_abstract":["FcγRIIB is an inhibitory receptor expressed throughout B cell development. Diminished expression or function is associated with lupus in mice and humans, in particular through an effect on autoantibody production and plasma cell (PC) differentiation. Here, we analyzed the effect of B cell-intrinsic FcγRIIB expression on B cell activation and PC differentiation. Loss of FcγRIIB on B cells in Fcgr2b-conditional KO (Fcgr2b-cKO) mice led to a spontaneous increase in autoantibody titers. This increase was most striking for IgG3, suggestive of increased extrafollicular responses. Marginal zone (MZ) B cells had the highest expression of FcγRIIB in both mice and humans. This high expression of FcγRIIB was linked to increased MZ B cell activation, Erk phosphorylation, and calcium flux in the absenc"],"journal":["The Journal of clinical investigation"],"pubmed_title":["FcγRIIB regulates autoantibody responses by limiting marginal zone B cell activation."],"pmcid":["PMC9435648"],"funding_grant_id":["P01 AI073693","1P01 AI073693","Research grant"],"pubmed_authors":["Kurata-Sato I","Diamond B","Malkiel S","Suurmond J","Dorjee AL","Barlev AN"],"additional_accession":[]},"is_claimable":false,"name":"FcγRIIB regulates autoantibody responses by limiting marginal zone B cell activation.","description":"FcγRIIB is an inhibitory receptor expressed throughout B cell development. Diminished expression or function is associated with lupus in mice and humans, in particular through an effect on autoantibody production and plasma cell (PC) differentiation. Here, we analyzed the effect of B cell-intrinsic FcγRIIB expression on B cell activation and PC differentiation. Loss of FcγRIIB on B cells in Fcgr2b-conditional KO (Fcgr2b-cKO) mice led to a spontaneous increase in autoantibody titers. This increase was most striking for IgG3, suggestive of increased extrafollicular responses. Marginal zone (MZ) B cells had the highest expression of FcγRIIB in both mice and humans. This high expression of FcγRIIB was linked to increased MZ B cell activation, Erk phosphorylation, and calcium flux in the absenc","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-04T09:02:49.405Z","creation":"2025-04-04T09:02:49.405Z"},"accession":"S-EPMC9435648","cross_references":{"pubmed":["35819855"],"doi":["10.1172/JCI157250"]}}