Abstract
Primary Sjögren's syndrome (pSS) is a chronic inflammatory autoimmune disease of exocrine gland. In pSS, permanent activation of the adaptive immune system is obvious. Lymphocyte co-stimulation plays an important part in inflammation and immunotherapy. Co-stimulator ligands (B7-H2) are significant costimulatory molecules. The interaction of B7-H2, with its sole receptor ICOS, promotes T cell differentiation, effector responses and activation. Our study found that B7-H2 is up-regulated in salivary gland, saliva and serum of pSS patients. B7-H2 expression in saliva have negatively correlated with saliva weight. Overexpression of B7-H2 into human salivary gland epithelial (HSGE) cells, increased the activity of p65 (phosphorylated at S536) and decreased the expression of AQP5. Furthermore, up-regulated B7-H2 induced apoptosis and inhibited proliferation in HSGE cell lines. These results suggest the expression of B7-H2 can decrease the secretion of saliva, increase the quantity of dental caries and reduce lifespan of patients of pSS.
Functional effects of proinflammatory factors present in Sjögren’s syndrome salivary microenvironment in an in vitro model of human salivary gland
