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The Dendritic Cell-Regulatory T Lymphocyte Crosstalk Contributes to Tumor-Induced Tolerance

机译:树突状细胞调节性T淋巴细胞串扰有助于肿瘤诱导的耐受性。

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摘要

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.
机译: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而逃避消除,其中包括有效抑制效应免疫细胞。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着重要作用。暴露于肿瘤衍生因子的分化树突状细胞(DCs)可能会在未成熟阶段被捕,在启动免疫反应时变得无能为力,并可能诱导效应T细胞无反应或缺失。这些产生耐受力的DC在不同类型的癌症患者中积累,也参与了Treg的产生。反过来,在肿瘤进展过程中扩展的Treg通过阻止DC协调免疫反应的能力以及直接抑制抗肿瘤T淋巴细胞来促进癌症的免疫耐受。本文中,我们回顾了DC和Treg之间的这些双向通讯,因为它们与促进癌症诱导的耐受性有关。

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