Cutting Edge: Central Nervous System Plasmacytoid Dendritic Cells Regulate the Severity of Relapsing Experimental Autoimmune Encephalomyelitis1
Cutting Edge: Central Nervous System Plasmacytoid Dendritic Cells Regulate the Severity of Relapsing Experimental Autoimmune Encephalomyelitis1
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最前沿：中枢神经系统浆细胞样树突状细胞调节复发性实验性自身免疫性脑脊髓炎的严重程度1
作者：
Samantha Bailey;Sarah C. Caulkins;G. Goings;Jens A. A. Fischer;A. Dzionek;S. Miller
浆细胞样树突状细胞（pDCs）对T细胞具有刺激和调节作用。pDCs是实验性自身免疫性脑脊髓炎中主要的中枢神经系统浸润树突状细胞群，但与髓系树突状细胞不同，它在T细胞活化和表位扩散中起次要作用。我们发现，在实验性自身免疫性脑脊髓炎的急性期或复发期，pDCs的消耗都会导致疾病严重程度的加剧。pDC耗竭可显著增强中枢神经系统，但不能增强外周CD4+ T细胞的活化，以及IL-17和IFN-γ的产生。此外，CNS pDCs以不依赖于ido的方式抑制CNS髓样树突状细胞驱动的IL-17、IFN-γ和IL-10的产生。这些数据表明，pDCs在负性调节致病性CNS CD4+ T细胞应答中发挥着关键的调节作用，突出了pDCs在炎症性自身免疫性疾病中的新作用。
Plasmacytoid dendritic cells (pDCs) have both stimulatory and regulatory effects on T cells. pDCs are a major CNS-infiltrating dendritic cell population during experimental autoimmune encephalomyelitis but, unlike myeloid dendritic cells, have a minor role in T cell activation and epitope spreading. We show that depletion of pDCs during either the acute or relapse phases of experimental autoimmune encephalomyelitis resulted in exacerbation of disease severity. pDC depletion significantly enhanced CNS but not peripheral CD4+ T cell activation, as well as IL-17 and IFN-γ production. Moreover, CNS pDCs suppressed CNS myeloid dendritic cell-driven production of IL-17, IFN-γ, and IL-10 in an IDO-independent manner. The data demonstrate that pDCs play a critical regulatory role in negatively regulating pathogenic CNS CD4+ T cell responses, highlighting a new role for pDCs in inflammatory autoimmune disease.
影响因子：
64.8
作者：
Lande, Roberto;Gregorio, Josh;Gilliet, Michel
通讯作者：
Gilliet, Michel