| First Author | Glatigny S | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 12 | Pages | 6176-9 |
| PubMed ID | 22084440 | Mgi Jnum | J:180388 |
| Mgi Id | MGI:5306191 | Doi | 10.4049/jimmunol.1102515 |
| Citation | Glatigny S, et al. (2011) Cutting edge: loss of alpha4 integrin expression differentially affects the homing of Th1 and Th17 cells. J Immunol 187(12):6176-9 |
| abstractText | The neutralization of alpha4 integrin is currently used as treatment in several autoimmune diseases and is thought to prevent the entry of most immune cells in target tissues. In this study, we showed that selective deletion of alpha4 integrin in T cells did not prevent but delayed the development of experimental autoimmune encephalomyelitis. Whereas both Th1 and Th17 cells infiltrate the CNS of wild-type mice, T cells present in the CNS of mice lacking alpha4 integrin were mainly enriched in Th17 cells, suggesting that this T cell subset uses other integrins to access the CNS. In contrast, alpha4 integrin expression is important for Th1 cells to enter the CNS and for the stability of their Th1-associated genetic program. Therefore, our data suggest that anti-alpha4 integrin Ab treatment may be more efficient in the treatment of Th1- rather than Th17-mediated disease. |
