Vav1-deficient mice are resistant to MOG-induced experimental autoimmune encephalomyelitis due to impaired antigen priming

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.