J Neuroimmunol. 2003 Jun;139(1-2):17-26
Korn T, Fischer KD, Girkontaite I, Kollner G, Toyka K, Jung S.
Department of Neurology, Neuroimmunology Branch and MS Clinical Research Group, Bayerische Julius-Maximilians-Universitat Wurzburg, Wurzburg, Germany
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.