Challenge with innate and protein antigens induces CCR7 expression by microglia in vitro and in vivo
Challenge with innate and protein antigens induces CCR7 expression by microglia in vitro and in vivo
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作者：
Dijkstra, I. M.;de Haas, A. H.;Biber, K.
由于活化的小胶质细胞能够吞噬受损细胞并随后表达主要组织相容性复合物II类（MHC-II）和共刺激蛋白，因此它们被认为在中枢神经系统中起抗原呈递细胞（APC）的作用。专职APC的成熟和迁移能力与趋化因子受体CCR 7的表达相关。因此，我们研究了小胶质细胞的免疫激活是否诱导CCR 7表达。我们在这里提出，激活培养的小胶质细胞的先天抗原脂多糖和蛋白抗原卵清蛋白迅速诱导CCR 7的表达，伴随着增加的MHC-II的表达。此外，它表明，在IBA-1阳性细胞中的CCR 7表达诱导的症状发作和发展的实验性自身免疫性脑脊髓炎，啮齿动物模型多发性硬化症。这些结果表明，小胶质细胞在特定的炎症条件下表达CCR 7，证实了小胶质细胞发育成具有向淋巴趋化因子迁移潜力的APC的观点。(c)2006 Wiley-Liss，Inc.
Since activated microglia are able to phagocytose damaged cells and subsequently express major histocompatibility complex class II (MHC-II) and co-stimulatory proteins, they are considered to function as antigen presenting cells (APCs) in the central nervous system. The maturation and migratory potential of professional APCs is associated with the expression of chemokine receptor CCR7. We therefore investigated whether the immunological activation of microglia induces CCR7 expression. We here present that activation of cultured microglia by both the innate antigen lipopolysaccharide and protein antigen ovalbumin rapidly induces CCR7 expression, accompanied by increased MHC-II expression. Moreover, it is shown that CCR7 expression in IBA-1 positive cells is induced during the symptom onset and progression of experimental autoimmune encephalomyelitis, a rodent model for multiple sclerosis. These results suggest that microglia express CCR7 under specific inflammatory conditions, corroborating the idea that microglia develop into APCs with migratory potential toward lymphoid chemokines. (c) 2006 Wiley-Liss, Inc.