Grewal I S, Foellmer H G, Grewal K D, Wang H, Lee W P, Tumas D, Janeway C A, Flavell R A
Department of Immunology, Genentech Incorporated, South San Francisco, CA 94080, USA.
Immunity. 2001 Mar;14(3):291-302. doi: 10.1016/s1074-7613(01)00110-8.
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.
黏附分子被认为有助于白细胞浸润到患有实验性自身免疫性脑脊髓炎（EAE）的小鼠中枢神经系统中。黏附分子CD62L（L-选择素）在EAE免疫病理学中的作用尚不清楚。为了研究这一点，我们将CD62L缺陷小鼠与髓鞘碱性蛋白特异性TCR（MBP-TCR）转基因小鼠进行杂交。CD62L缺陷的MBP-TCR转基因小鼠未能发生抗原诱导的EAE，并且尽管存在白细胞浸润，但在中枢神经系统中未观察到髓鞘损伤。然而，在过继转移野生型巨噬细胞后，CD62L缺陷小鼠可诱导出EAE。我们的结果表明，CD62L对于自身免疫性CD4 T细胞的激活不是必需的，但对于中枢神经系统中效应细胞的最终破坏功能很重要，并支持一种新机制，即效应细胞上表达的CD62L在介导髓鞘损伤中起重要作用。
