| First Author | Korn T | Year | 2003 |
| Journal | J Neuroimmunol | Volume | 139 |
| Issue | 1-2 | Pages | 17-26 |
| PubMed ID | 12799016 | Mgi Jnum | J:119041 |
| Mgi Id | MGI:3701042 | Doi | 10.1016/s0165-5728(03)00128-0 |
| Citation | Korn T, et al. (2003) Vav1-deficient mice are resistant to MOG-induced experimental autoimmune encephalomyelitis due to impaired antigen priming. J Neuroimmunol 139(1-2):17-26 |
| abstractText | Mice that lack the guanine nucleotide exchange factor (GEF) Vav1 exhibit particular defects in antigen-triggered T cell activation but may have an autoreactive T cell repertoire due to impaired intra-thymic negative selection. MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE) was used to test the susceptibility of Vav1(-/-) mice to organ-specific autoimmunity. Vav1(-/-) animals were found to be resistant to MOG(35-55)-EAE since the priming and in vivo expansion of myelin oligodendrocyte glycoprotein (MOG)-specific T cells was inefficient despite fully functional antigen presentation. Protection from cell-mediated autoimmunity was not due to a Th2 bias, to the lack of IL-2 or a failure of Vav1(-/-) T cells in terms of chemotactic mobility. |
