{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Brian BF"],"funding":["NCI NIH HHS","NIAMS NIH HHS"],"pagination":["eabj5227"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9032976"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(16)"],"pubmed_abstract":["Here, we report that the LynB splice variant of the Src-family kinase Lyn exerts a dominant immunosuppressive function in vivo, whereas the LynA isoform is uniquely required to restrain autoimmunity in female mice. We used CRISPR-Cas9 gene editing to constrain <i>lyn</i> splicing and expression, generating single-isoform LynA knockout (LynA<sup>KO</sup>) or LynB<sup>KO</sup> mice. Autoimmune disease in total Lyn<sup>KO</sup> mice is characterized by production of antinuclear antibodies, glomerulonephritis, impaired B cell development, and overabundance of activated B cells and proinflammatory myeloid cells. Expression of LynA or LynB alone uncoupled the developmental phenotype from the autoimmune disease: B cell transitional populations were restored, but myeloid cells and differentiated B"],"journal":["Science advances"],"pubmed_title":["A dominant function of LynB kinase in preventing autoimmunity."],"pmcid":["PMC9032976"],"funding_grant_id":["R01 AR073966","T32 CA009138","P30 CA077598"],"pubmed_authors":["Sauer ML","Greene JT","Binstadt BA","Funk OL","Ramirez LA","Auger JL","Nunez MG","Moriarity BS","Freedman TS","Brian BF","Lindstedt AJ","Lowell CA","Swanson WL","Senevirathne SE","Ruis BL"],"additional_accession":[]},"is_claimable":false,"name":"A dominant function of LynB kinase in preventing autoimmunity.","description":"Here, we report that the LynB splice variant of the Src-family kinase Lyn exerts a dominant immunosuppressive function in vivo, whereas the LynA isoform is uniquely required to restrain autoimmunity in female mice. We used CRISPR-Cas9 gene editing to constrain <i>lyn</i> splicing and expression, generating single-isoform LynA knockout (LynA<sup>KO</sup>) or LynB<sup>KO</sup> mice. Autoimmune disease in total Lyn<sup>KO</sup> mice is characterized by production of antinuclear antibodies, glomerulonephritis, impaired B cell development, and overabundance of activated B cells and proinflammatory myeloid cells. Expression of LynA or LynB alone uncoupled the developmental phenotype from the autoimmune disease: B cell transitional populations were restored, but myeloid cells and differentiated B","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2025-04-19T08:21:17.789Z","creation":"2024-11-21T06:15:47.479Z"},"accession":"S-EPMC9032976","cross_references":{"pubmed":["35452291"],"doi":["10.1126/sciadv.abj5227"]}}