Abstract
The αLβ2 integrin adhesion molecule LFA-1 is believed to be involved in the migration of autoreactive T cells to the central nervous system across the endothelial blood–brain barrier in experimental autoimmune encephalomyelitis (EAE). Here, we demonstrate that the incidence and clinical scores of EAE in LFA-1 −/− mice induced by the immunization with the myelin oligodendrocyte glycoprotein (MOG)-peptide antigen were significantly lower than those in wild type mice. Further studies demonstrated that lymphocytes recruitment to the draining lymph nodes (dLN) after the immunization with the MOG-peptide was severely suppressed in LFA-1 −/− mice. Moreover, generation of the MOG-specific IL-17-producing helper T (Th17) cells in the dLN was impaired in LFA-1 −/− mice. These results suggest that LFA-1 may play an important role for the generation of MOG-specific Th17 cells in the dLN as well as the immigration of MOG-specific naïve CD4 + T cells to the dLN.
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