The dendritic cell-regulatory T lymphocyte crosstalk contributes to tumor-induced tolerance.
The dendritic cell-regulatory T lymphocyte crosstalk contributes to tumor-induced tolerance.
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DOI：
10.1155/2011/430394
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发表时间：
2011
影响因子：
--
通讯作者：
Larmonier N
中科院分区：
文献类型：
--
作者：
Janikashvili N;Bonnotte B;Katsanis E;Larmonier N
肿瘤细胞通常使用多种策略通过先天性和适应性免疫应答逃避消除，其中包括主动抑制效应免疫细胞。调节性T淋巴细胞（Treg）和致耐受性树突状细胞在癌症诱导的免疫抑制的建立和持续中起重要作用。暴露于肿瘤源性因子的分化树突状细胞（DC）可在不成熟阶段被阻止，从而在启动免疫应答时变得无能，并且可诱导效应T细胞无反应性或缺失。这些致耐受性DC在患有不同类型癌症的患者中积累，也参与Treg的产生。反过来，在肿瘤进展期间扩增的Treg通过阻碍DC协调免疫应答的能力和通过直接抑制抗肿瘤T淋巴细胞而有助于癌症的免疫耐受。在此，我们回顾这些DC和Treg之间的双向通信，因为它们与促进癌症诱导的耐受性有关。
Tumor cells commonly escape from elimination by innate and adaptive immune responses using multiple strategies among which is the active suppression of effector immune cells. Regulatory T lymphocytes (Treg) and tolerogenic dendritic cells play essential roles in the establishment and persistence of cancer-induced immunosuppression. Differentiating dendritic cells (DCs) exposed to tumor-derived factors may be arrested at an immature stage becoming inept at initiating immune responses and may induce effector T-cell anergy or deletion. These tolerogenic DCs, which accumulate in patients with different types of cancers, are also involved in the generation of Treg. In turn, Treg that expand during tumor progression contribute to the immune tolerance of cancer by impeding DCs' ability to orchestrate immune responses and by directly inhibiting antitumoral T lymphocytes. Herein we review these bidirectional communications between DCs and Treg as they relate to the promotion of cancer-induced tolerance.
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