| First Author | Ma J | Year | 2016 |
| Journal | Am J Pathol | Volume | 186 |
| Issue | 6 | Pages | 1559-67 |
| PubMed ID | 27106763 | Mgi Jnum | J:233685 |
| Mgi Id | MGI:5787857 | Doi | 10.1016/j.ajpath.2016.02.010 |
| Citation | Ma J, et al. (2016) Blockade of Glucocorticoid-Induced Tumor Necrosis Factor-Receptor-Related Protein Signaling Ameliorates Murine Collagen-Induced Arthritis by Modulating Follicular Helper T Cells. Am J Pathol 186(6):1559-67 |
| abstractText | Recent studies have shown that glucocorticoid-induced tumor necrosis factor-receptor-related protein (GITR) and its ligand (GITRL) are critically involved in the pathogenesis of autoimmune arthritis, but the role of GITRL/GITR signaling in modulating CD4(+) follicular helper T (Tfh) cell response during autoimmune arthritis remains largely unclear. We showed that splenic Tfh cells from mice with collagen-induced arthritis expressed higher levels of GITR compared with non-Tfh cells. In vitro, GITRL treatment markedly enhanced the percentage and number of Tfh cells. The administration of GITR fused to fragment crystallizable of IgG protein in mice with collagen-induced arthritis suppressed the Tfh cell response, resulting in ameliorated disease severity, and reduced production of autoantibody and the number of autoantibody-secreting cells in both the spleen and bone marrow. Together, these results indicate that blockade of GITR signaling can ameliorate arthritis progression mainly by modulating the Tfh cell response. |
