Expression of Gαq Is Decreased in Lymphocytes from Primary Sjögren's Syndrome Patients and Related to Increased IL-17A Expression. (7th June 2018)

• Record Type: Journal Article
• Authors: Sun, Yuechi; Wang, Ying; Chen, Shiju; Fan, Guihua; Zhang, Junhui; Dai, Fan; Qian, Hongyan; Liu, Yuan; Shi, Guixiu
• Other Names: Rao Xiaoquan Academic Editor.
• Is Part Of: Journal of immunology research. Volume 2018(2018)
• Publication Date: 2018-06-07
• Subjects: Immunology -- Periodicals; Immunology -- Research -- Periodicals; 616.07905
• DOI: 10.1155/2018/8212641
• Languages: English
• ISSNs: 2314-8861

Abstract

Abstract : Primary Sjögren's syndrome (pSS) is a rheumatic disease characterized by the destruction of salivary and lacrimal glands, and its pathogenesis mechanism remains unclear. G α q is the α -subunit of the heterotrimeric Gq protein. Researches demonstrated that G α q was involved in the pathogenesis regulation of several rheumatic diseases. This study explored the role of G α q in pSS. G α q mRNA levels in peripheral blood mononuclear cells (PBMCs) from 39 patients and 26 healthy controls (HCs) were investigated using real-time PCR. IL-17A serum concentrations in 22 pSS patients and 23 HCs were tested by ELISA, and the clinical significance of G α q was analyzed. The association of G α q with interleukin-17A (IL-17A) expression was also analyzed in patients with pSS. We showed that G α q expression in PBMCs from patients with pSS was significantly lower than that in PBMCs from HCs. G α q expression level was closely associated with pSS disease activity. Furthermore, a negative association was also found in IL-17A and G α q expression level. These data suggest that G α q is involved in pSS pathogenesis regulation, possibly due to its regulation of Th17. These results provide new insights into the pSS pathogenesis mechanism involving abnormal Th17 regulation.