{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["5(1)"],"submitter":["Hodgson R"],"funding":["Kidney Research UK","RCUK | Medical Research Council"],"pubmed_abstract":["Peripheral tolerance prevents the initiation of damaging immune responses by autoreactive lymphocytes. While tolerogenic mechanisms are tightly regulated by antigen-dependent and independent signals, downstream pathways are incompletely understood. N-myc downstream-regulated gene 1 (NDRG1), an anti-cancer therapeutic target, has previously been implicated as a CD4<sup>+</sup> T cell clonal anergy factor. By RNA-sequencing, we identified Ndrg1 as the third most upregulated gene in anergic, compared to naïve follicular, B cells. Ndrg1 is upregulated by B cell receptor activation (signal one) and suppressed by co-stimulation (signal two), suggesting that NDRG1 may be important in B cell tolerance. However, though Ndrg1<sup>-/-</sup> mice have a neurological defect mimicking NDRG1-associated Charcot-Marie-Tooth (CMT4d) disease, primary and secondary immune responses were normal. We find that B cell tolerance is maintained, and NDRG1 does not play a role in downstream responses during re-stimulation of in vivo antigen-experienced CD4<sup>+</sup> T cells, demonstrating that NDGR1 is functionally redundant for lymphocyte anergy."],"journal":["Communications biology"],"pagination":["1216"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9649591"],"repository":["biostudies-literature"],"pubmed_title":["NDRG1 is induced by antigen-receptor signaling but dispensable for B and T cell self-tolerance."],"pmcid":["PMC9649591"],"pubmed_authors":["Bhandari A","Hodgson R","Crockford TL","Deobagkar-Lele M","Anzilotti C","Bull KR","Wilcock MJ","Cebrian-Serrano A","Kepple JD","Xu X","Cawthorne E","Cornall RJ","Davies B"],"additional_accession":[]},"is_claimable":false,"name":"NDRG1 is induced by antigen-receptor signaling but dispensable for B and T cell self-tolerance.","description":"Peripheral tolerance prevents the initiation of damaging immune responses by autoreactive lymphocytes. While tolerogenic mechanisms are tightly regulated by antigen-dependent and independent signals, downstream pathways are incompletely understood. N-myc downstream-regulated gene 1 (NDRG1), an anti-cancer therapeutic target, has previously been implicated as a CD4<sup>+</sup> T cell clonal anergy factor. By RNA-sequencing, we identified Ndrg1 as the third most upregulated gene in anergic, compared to naïve follicular, B cells. Ndrg1 is upregulated by B cell receptor activation (signal one) and suppressed by co-stimulation (signal two), suggesting that NDRG1 may be important in B cell tolerance. However, though Ndrg1<sup>-/-</sup> mice have a neurological defect mimicking NDRG1-associated Charcot-Marie-Tooth (CMT4d) disease, primary and secondary immune responses were normal. We find that B cell tolerance is maintained, and NDRG1 does not play a role in downstream responses during re-stimulation of in vivo antigen-experienced CD4<sup>+</sup> T cells, demonstrating that NDGR1 is functionally redundant for lymphocyte anergy.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Nov","modification":"2024-11-20T15:23:07.402Z","creation":"2024-11-20T15:23:07.402Z"},"accession":"S-EPMC9649591","cross_references":{"pubmed":["36357486"],"doi":["10.1038/s42003-022-04118-w"]}}