Dendritic cells as targets for therapy in rheumatoid arthritis.
Dendritic cells as targets for therapy in rheumatoid arthritis.
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DOI：
10.1038/nrrheum.2009.185
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发表时间：
2009-10
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影响因子：
--
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中科院分区：
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--
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树突状细胞（DC）作为专职抗原呈递细胞（APC）在免疫诱导和耐受中发挥核心作用。在没有DC的情况下，在动物模型中发展致命的自身免疫。虽然DC在风湿性关节炎（RA）发病机制中的作用已被广泛研究，但DC是否在该疾病中启动自身免疫仍不清楚。然而，证据表明，DC在其维持和发展中起着重要作用。目前RA的生物治疗旨在通过靶向APC的下游产物如TNFα、IL-1和IL-6来改善疾病。RA的新兴疗法正在利用DC的致耐受能力。“致耐受性”DC可以从骨髓前体离体产生，负载有抗原并通过诱导活化诱导的细胞死亡（AICD）、无反应性和/或调节性T细胞来操纵以抑制体内自身免疫应答。由DC致敏的细胞，如B细胞、辅助性T（Th）-1（Th 1）和Th 17细胞，以及在某些自身免疫模型中涉及的细胞，也被认为是基于免疫的治疗的另外的靶标。在这些方法应用于临床之前，有必要进行研究以验证它们改善自身免疫的方法。
Dendritic cells (DC) play a central role in the induction of immunity and also in tolerance in their role as professional antigen-presenting cells (APC). In the absence of DC, a fatal autoimmunity develops in animal models. While the role of DC has been investigated extensively in the pathogenesis of Rheumatoid arthritis (RA), it remains unclear if DC initiate autoimmunity in this disease. Nevertheless, evidence points towards a significant role for DC in its maintenance and progression. Current biological therapies of RA are designed to ameliorate disease by targeting downstream products of APC such as TNFα, IL-1 and IL-6. Emerging therapies for RA are exploiting the tolerogenic capacity of DC. “Tolerogenic” DC can be generated from myeloid precursors ex vivo, loaded with antigen and manipulated to suppress autoimmune responses in vivo, through the induction of activation induced cell death (AICD), anergy, and/or regulatory T cells. Cells that are primed by DC such as B cells, T helper (Th)-1(Th1) and Th17 cells, and which have been implicated in certain models of autoimmunity, are also being considered as additional targets for immune based therapy. Studies to validate these approaches to ameliorate autoimmunity will be necessary before they are applied in the clinic.
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影响因子：
32.4
作者：
Jung, S;Unutmaz, D;Lang, RA
通讯作者：
Lang, RA
影响因子：
27.4
作者：
Brentano, F.;Ospelt, C.;Kyburz, D.
通讯作者：
Kyburz, D.
影响因子：
100.3
作者：
Bluestone, Jeffrey A.;Thomson, Angus W.;Weiner, Howard L.
通讯作者：
Weiner, Howard L.
影响因子：
15.3
作者：
Dhodapkar, M V;Steinman, R M;Krasovsky, J;Munz, C;Bhardwaj, N
通讯作者：
Bhardwaj, N
影响因子：
4.9
作者：
Jongbloed, SL;Lebre, MC;McInnes, IB
通讯作者：
McInnes, IB