{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liao Y"],"funding":["Laboratory of Lingnan Mordern Agriculture Project","National key R&amp;D Program of China","National Natural Science Foundation of China"],"pagination":["e2215921119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9636909"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(44)"],"pubmed_abstract":["Recent compelling results indicate possible links between neurotransmitters, intestinal mucosal IgA<sup>+</sup> B cell responses, and immunoglobulin A nephropathy (IgAN) pathogenesis. Here, we demonstrated that γ-amino butyric acid (GABA) transporter-2 (GAT-2) deficiency induces intestinal germinal center (GC) B cell differentiation and worsens the symptoms of IgAN in a mouse model. Mechanistically, GAT-2 deficiency enhances GC B cell differentiation through activation of GABA-mammalian target of rapamycin complex 1 (mTORC1) signaling. In addition, IgAN patients have lower GAT-2 expression but higher activation of mTORC1 in blood B cells, and both are correlated with kidney function in IgAN patients. Collectively, this study describes GABA signaling-mediated intestinal mucosal immunity as "],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["GABA signaling enforces intestinal germinal center B cell differentiation."],"pmcid":["PMC9636909"],"funding_grant_id":["2021YFD1300700","NT2021005","31872365"],"pubmed_authors":["Duan J","Yin Y","Liao Y","Cai Q","Ren W","Chen Q","Bin P","Hu X","Han W","Zhu C","Ding S","Zhang Y","Fan L","Cai Y"],"additional_accession":[]},"is_claimable":false,"name":"GABA signaling enforces intestinal germinal center B cell differentiation.","description":"Recent compelling results indicate possible links between neurotransmitters, intestinal mucosal IgA<sup>+</sup> B cell responses, and immunoglobulin A nephropathy (IgAN) pathogenesis. Here, we demonstrated that γ-amino butyric acid (GABA) transporter-2 (GAT-2) deficiency induces intestinal germinal center (GC) B cell differentiation and worsens the symptoms of IgAN in a mouse model. Mechanistically, GAT-2 deficiency enhances GC B cell differentiation through activation of GABA-mammalian target of rapamycin complex 1 (mTORC1) signaling. In addition, IgAN patients have lower GAT-2 expression but higher activation of mTORC1 in blood B cells, and both are correlated with kidney function in IgAN patients. Collectively, this study describes GABA signaling-mediated intestinal mucosal immunity as ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2026-07-14T16:57:37.642Z","creation":"2025-04-06T08:02:52.008Z"},"accession":"S-EPMC9636909","cross_references":{"pubmed":["36279432"],"doi":["10.1073/pnas.2215921119"]}}