Measles virus and dendritic cell functions: how specific response cohabits with immunosuppression.

Measles virus and dendritic cell functions: how specific response cohabits with immunosuppression.
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麻疹病毒和树突状细胞功能:特异性反应如何与免疫抑制共存。

DOI:
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发表时间:
2003
影响因子:
--
通讯作者:
C. Rabourdin
C. Rabourdin
中科院分区:
医学3区
文献类型:
--
作者:
C. Servet‐Delprat;P. Vidalain;H. Valentin;C. Rabourdin

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麻疹病毒(MV)感染诱导有效的MV特异性免疫应答和短暂但深刻的免疫抑制,其特征在于泛淋巴细胞减少症,其偶尔导致机会性感染,导致儿童的高死亡率。在体外研究的基础上,树突状细胞(DC)在MV感染中的假定作用进行了讨论。(1)DC可以参与抗MV的天然免疫,因为MV开启了TNF相关凋亡诱导配体(TRAIL)介导的DC细胞毒性。(2)未感染DC的交叉致敏可能是MV适应性免疫应答的途径。(3)在次级淋巴器官中CD 40-配体活化后,MV感染的DC可以启动Warthin-Finkeldey多核巨细胞的形成,复制MV并负责MV的体内传播。(4)我们回顾如何整合病毒攻击宿主免疫系统也靶向DC:在了解MV感染的DC,可以解释MV诱导的免疫抑制在体内观察到的免疫生物学的进展,并强调其在淋巴细胞减少症的潜在作用。最后,提出了今后的研究方向。
Measles virus (MV) infection induces both an efficient MV-specific immune response and a transient but profound immunosuppression characterised by a panlymphopenia that occasionally results in opportunistic infections responsible for a high rate of mortality in children. On the basis of in vitro studies, the putative roles of dendritic cells (DCs) in MV infection are discussed. (1) DCs could participate in anti-MV innate immunity because MV turns on TNF-related apoptosis-inducing ligand (TRAIL)-mediated DC cytotoxicity. (2) Cross-priming by non-infected DCs might be the route of MV adaptive immune response. (3) After CD40-ligand activation in secondary lymphoid organs, MV-infected DCs could initiate the formation of Warthin-Finkeldey multinucleated giant cells, replicating MV and responsible for in vivo spreading of MV. (4) We review how integrated viral attack of the host immune system also targets DCs: Progress in understanding the immunobiology of MV-infected DCs that could account for MV-induced immunosuppression observed in vivo is presented and their potential role in lymphopenia is underlined. In conclusion, future research directions are proposed.
麻疹病毒疫苗接种后细胞因子产生的变化:IL-4 的主要产生表明诱导了 Th2 反应。
DOI: 10.1006/clin.1993.1061
发表时间: 1993
期刊: Clinical immunology and immunopathology
影响因子: --
作者:
Ward,BJ;Griffin,DE
通讯作者: Griffin,DE