CD62L is required for the priming of encephalitogenic T cells but does not play a major role in the effector phase of experimental autoimmune encephalomyelitis.

CD62L (l-selectin, mel 14) regulates naïve T cell homing into lymph nodes and the migration of leucocytes to sites of inflammation. The requirement of CD62L in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, has been demonstrated previously. However, it remains controversial as to whether CD62L is required for the induction or the effector phase of EAE. It is also unclear whether other non-T effector cells need CD62L to enter the central nervous system (CNS) parenchyma and exert their damaging effects on myelin. We report that mice with a targeted mutation of CD62L are resistant to Myelin oligodendrocyte glycoprotein peptide-induced EAE. CD62L-deficient mice had no peptide-specific T cell responses in the draining lymph nodes and had lower levels of peptide-specific T cell responses in spleens at a later time point. Adoptive transfer studies showed that CD62L-deficient mice were fully susceptible to adoptive transfer EAE induced by either wildtype or CD62L-deficient T cells. Moreover, CD62L-deficient, F4/80(+) macrophages can be efficiently recruited into the CNS parenchyma. These data suggest that CD62L is required for the induction of encephalitogenic T cells during EAE development, but is not required by T and non-T effector cells to attack the CNS parenchyma.