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SJL/L-selectin-deficient mice develop experimental autoimmune encephalomyelitis
The role of L-selectin in the pathogenesis of EAE is still not clarified and previous investigations were not conclusive. To address whether L-selectin is involved in the development of EAE, SJL/L-sel-/- mice were generated backcrossing L-selectin-deficient mice into the SJL mouse strain. EAE was induced by active immunization with proteolipid protein (PLP). SJL wt and SJL/L-sel-/- mice had indistinguishable EAE symptoms and in brain of EAE affected mice CD45 + cell infiltrates were detected. EAE by adoptive transfer of in vitro activated PLP-specific T cell blasts was also induced, and in both strains EAE symptoms were scored and was possible to detect CD45+ cell infiltrates in brain and spinal cord. The migration efficiency of SJL wt and SJL/L-sel-/- T cells across the endothelium was evaluated by a functional assay. Taken together, it is possible to conclude that L-selectin is not involved in the recruitment of encephalitogenic cells across the BBB and in the pathogenesis of EAE in SJL mice.