| First Author | Wang D | Year | 2017 |
| Journal | Mediators Inflamm | Volume | 2017 |
| Pages | 4639081 | PubMed ID | 28197018 |
| Mgi Jnum | J:326317 | Mgi Id | MGI:6863372 |
| Doi | 10.1155/2017/4639081 | Citation | Wang D, et al. (2017) Galphaq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation. Mediators Inflamm 2017:4639081 |
| abstractText | The Galphaq-containing G protein, an important member of Gq/11 class, is ubiquitously expressed in mammalian cells. Galphaq has been found to play an important role in immune regulation and development of autoimmune disease such as rheumatoid arthritis (RA). However, how Galphaq participates in the pathogenesis of RA is still not fully understood. In the present study, we aimed to find out whether Galphaq controls RA via regulation of Th1 differentiation. We observed that the expression of Galphaq was negatively correlated with the expression of signature Th1 cytokine (IFN-gamma) in RA patients, which suggests a negative role of Galphaq in differentiation of Th1 cells. By using Galphaq knockout (Gnaq-/-) mice, we demonstrated that loss of Galphaq led to enhanced Th1 cell differentiation. Galphaq negative regulated the differentiation of Th1 cell by modulating the expression of T-bet and the activity of STAT4. Furthermore, we detected the increased ratio of Th1 cells in Gnaq-/- bone marrow (BM) chimeras spontaneously developing inflammatory arthritis. In conclusion, results presented in the study demonstrate that loss of Galphaq promotes the differentiation of Th1 cells and contributes to the pathogenesis of RA. |
