Details

Autor(en) / Beteiligte

• Xu, Ting
• Xie, Wen
• Ma, Yingchun
• Zhou, Shiliang
• Zhang, Lu
• Chen, Jinyun
• Cai, Mingyuan
• Sun, Rurong
• Zhang, Peirong
• Yu, Shaobo
• Xu, Zheng
• Jiang, Wanlan
• Wu, Min

Titel

Leptin/OB-R pathway promotes IL-4 secretion from B lymphocytes and induces salivary gland epithelial cell apoptosis in Sjögren's syndrome

Ist Teil von

• Oncotarget, 2017-09, Vol.8 (38), p.63417-63429

Ort / Verlag

United States: Impact Journals LLC

Erscheinungsjahr

2017

Link zum Volltext

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 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.