| First Author | Wang J | Year | 2018 |
| Journal | Acta Biochim Biophys Sin (Shanghai) | Volume | 50 |
| Issue | 7 | Pages | 666-675 |
| PubMed ID | 29860267 | Mgi Jnum | J:279090 |
| Mgi Id | MGI:6359673 | Doi | 10.1093/abbs/gmy060 |
| Citation | Wang J, et al. (2018) Gpr97/Adgrg3 ameliorates experimental autoimmune encephalomyelitis by regulating cytokine expression. Acta Biochim Biophys Sin (Shanghai) 50(7):666-675 |
| abstractText | Multiple sclerosis and its primary animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory diseases of the central nervous system (CNS) characterized by immune-mediated demyelination and neurodegeneration that may be mediated by inhibition of the nuclear factor-kappaB (NF-kappaB) signaling pathway. Gpr97, encoded by Adgrg3, has been reported to regulate the activity of NF-kappaB. In this study, using a previously established Adgrg3-knockout mouse model, we investigated the roles of Gpr97 in the development of autoimmune CNS disease in mice. We found a marked increase in the expression of Adgrg3 in spinal cords of mice with EAE. Adgrg3-deficient (Adgrg3-/-) mice with EAE exhibited increases in peak severity and the cumulative disease score compared with littermate controls, followed by a notable increase of leukocyte infiltration and more extensive demyelination. The percentages of Th1/Th17 cells in the CNS were significantly increased in Adgrg3-/- mice and accompanied by high levels of interleukin (IL)-6, interferon-gamma, tumor necrosis factor-alpha, and IL-17. An in vitro culture assay verified that Gpr97 regulated proinflammatory cytokine production. Taken together, our results show that Gpr97 plays an important role in the development of EAE and may have a therapeutic potential for the treatment of CNS autoimmunity. |
