Deshpande Pratima, King Irah L, Segal Benjamin M
Department of Microbiology and Immunology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA.
J Immunol. 2007 Jun 1;178(11):6695-9. doi: 10.4049/jimmunol.178.11.6695.
CD11c(+) dendritic cells (DCs) are a prominent component of CNS infiltrates in mice with experimental autoimmune encephalomyelitis. However, their role in immunopathogenesis is controversial. In this study, we report that they originate from peripheral hemopoietic cells and exhibit diverse functions that change during the course of acute disease. CNS DCs stimulate naive T cells to proliferate and polarize Th(17) responses when harvested shortly following disease onset but are relatively inefficient APC by the time of peak disability. Conversely, they can support CD4(+)CD25(+) T cell-mediated immunosuppression early during experimental autoimmune encephalomyelitis. Such paradoxical functions might reflect dual roles of CNS DCs in promoting local inflammation while setting the stage for remission.
在患有实验性自身免疫性脑脊髓炎的小鼠中，CD11c(+)树突状细胞（DCs）是中枢神经系统浸润的主要成分。然而，它们在免疫发病机制中的作用存在争议。在本研究中，我们报告它们起源于外周造血细胞，并表现出在急性疾病过程中发生变化的多种功能。疾病发作后不久收获的中枢神经系统DCs刺激幼稚T细胞增殖并极化Th(17)反应，但在残疾高峰期时它们作为抗原呈递细胞（APC）的效率相对较低。相反，在实验性自身免疫性脑脊髓炎早期，它们可以支持CD4(+)CD25(+) T细胞介导的免疫抑制。这种矛盾的功能可能反映了中枢神经系统DCs在促进局部炎症同时为缓解奠定基础方面的双重作用。
