| First Author | Grewal IS | Year | 2001 |
| Journal | Immunity | Volume | 14 |
| Issue | 3 | Pages | 291-302 |
| PubMed ID | 11290338 | Mgi Jnum | J:68349 |
| Mgi Id | MGI:1932594 | Doi | 10.1016/s1074-7613(01)00110-8 |
| Citation | Grewal IS, et al. (2001) CD62L is required on effector cells for local interactions in the CNS to cause myelin damage in experimental allergic encephalomyelitis. Immunity 14(3):291-302 |
| abstractText | Adhesion molecules are believed to facilitate infiltration of leukocytes into the CNS of mice with experimental allergic encephalomyelitis (EAE). The role of the adhesion molecule CD62L (L-selectin) in the immunopathology of EAE is not known. To study this, we crossed CD62L-deficient mice with myelin basic protein-specific TCR (MBP-TCR) transgenic mice. CD62L-deficient MBP-TCR transgenic mice failed to develop antigen-induced EAE, and, despite the presence of leukocyte infiltration, damage to myelin in the CNS was not seen. EAE could, however, be induced in CD62L-deficient mice upon adoptive transfer of wild-type macrophages. Our results suggest that CD62L is not required for activation of autoimmune CD4 T cells but is important for the final destructive function of effector cells in the CNS and support a novel mechanism whereby CD62L expressed on effector cells is important in mediating myelin damage. |
