| First Author | Zhao Z | Year | 2010 |
| Journal | Int Immunol | Volume | 22 |
| Issue | 10 | Pages | 817-26 |
| PubMed ID | 20679513 | Mgi Jnum | J:164321 |
| Mgi Id | MGI:4831094 | Doi | 10.1093/intimm/dxq432 |
| Citation | Zhao Z, et al. (2010) Targeting ganglioside epitope 3G11 on the surface of CD4+ T cells suppresses EAE by altering the Treg/Th17 cell balance. Int Immunol 22(10):817-26 |
| abstractText | Loss of expression of the 3G11 epitope, present on disialoceramide that is predominantly found on CD4(+) T cells, has been associated with a regulatory T cell (Treg) phenotype and tolerance induction in experimental autoimmune encephalomyelitis (EAE). Here we report that treatment with anti-3G11 mAb shifts the immune response from pro-inflammatory to tolerogenic and suppresses both chronic-progressive and relapsing-remitting EAE. This therapeutic effect can be achieved at different stages of EAE. Treatment with anti-3G11 mAb increased the proportion of Foxp3(+)CD25(+)CD4(+) Tregs and IL-10 production while inhibiting production of pro-inflammatory cytokines and responsiveness to IL-2 and decreasing the proportion of T(h)17 cells. The effect of anti-3G11 mAb was diminished in IL-10(-/-) mice, indicating that this cytokine mediates some of its effects. As 3G11 belongs to the ganglioside family, which is expressed on the surface of both murine and human CD4(+) T cells, targeting this class of molecules may provide a novel approach for treating autoimmune diseases. |
