{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8(38)"],"submitter":["Xu T"],"pubmed_abstract":["Sjögren's syndrome (SjS) is a chronic autoimmune epithelitis in which cell apoptosis promotes the formation of inflammatory lesions. We used immunohistochemistry and TUNEL to assay B cell infiltration and apoptosis in salivary gland tissue from 16-week-old NOD/LtJ mice with SjS. In co-cultures of primary salivary glandepithelial cells (SGECs) and spleen B cells, we assessed SGEC viability and apoptosis using CCK8 assays and flow cytometry. ELISAs were employed to assess cytokine levels in culture medium. Leptin protein, leptin receptor (OB-R), pro- and anti-apoptotic proteins, and Jak2/Stat3/ERK signaling molecules were analyzed using western blotting. B cell infiltration and salivary gland apoptosis were increased in salivary tissue from mice with SjS. Leptin treatment had no effect on cell viability or apoptosis among B cells and primary SGECs. B cell and SGEC co-culture systems showed that leptin increased apoptosis induced by B lymphocytes, reduced SGEC cell viability, and promoted IL-4 secretion from B cells. This suggests Leptin/OB-R signaling stimulates B cells-induced SGEC apoptosis via IL-4 secretion and OB-R-Jak2-Stat3 activation."],"journal":["Oncotarget"],"pagination":["63417-63429"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5609933"],"repository":["biostudies-literature"],"pubmed_title":["Leptin/OB-R pathway promotes IL-4 secretion from B lymphocytes and induces salivary gland epithelial cell apoptosis in Sjogren's syndrome."],"pmcid":["PMC5609933"],"pubmed_authors":["Xie W","Wu M","Chen J","Cai M","Yu S","Zhou S","Ma Y","Zhang L","Zhang P","Sun R","Jiang W","Xu T","Xu Z"],"additional_accession":[]},"is_claimable":false,"name":"Leptin/OB-R pathway promotes IL-4 secretion from B lymphocytes and induces salivary gland epithelial cell apoptosis in Sjogren's syndrome.","description":"Sjögren's syndrome (SjS) is a chronic autoimmune epithelitis in which cell apoptosis promotes the formation of inflammatory lesions. We used immunohistochemistry and TUNEL to assay B cell infiltration and apoptosis in salivary gland tissue from 16-week-old NOD/LtJ mice with SjS. In co-cultures of primary salivary glandepithelial cells (SGECs) and spleen B cells, we assessed SGEC viability and apoptosis using CCK8 assays and flow cytometry. ELISAs were employed to assess cytokine levels in culture medium. Leptin protein, leptin receptor (OB-R), pro- and anti-apoptotic proteins, and Jak2/Stat3/ERK signaling molecules were analyzed using western blotting. B cell infiltration and salivary gland apoptosis were increased in salivary tissue from mice with SjS. Leptin treatment had no effect on cell viability or apoptosis among B cells and primary SGECs. B cell and SGEC co-culture systems showed that leptin increased apoptosis induced by B lymphocytes, reduced SGEC cell viability, and promoted IL-4 secretion from B cells. This suggests Leptin/OB-R signaling stimulates B cells-induced SGEC apoptosis via IL-4 secretion and OB-R-Jak2-Stat3 activation.","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Sep","modification":"2022-02-09T09:24:52.313Z","creation":"2019-03-27T02:57:09Z"},"accession":"S-EPMC5609933","cross_references":{"pubmed":["28969001"],"doi":["10.18632/oncotarget.18823"]}}