Janikashvili Nona, Bonnotte Bernard, Katsanis Emmanuel, Larmonier Nicolas
Faculty of Medicine, INSERM UMR 866, IFR 100, 21000 Dijon, France.
Clin Dev Immunol. 2011;2011:430394. doi: 10.1155/2011/430394. Epub 2011 Nov 3.
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.
肿瘤细胞通常通过多种策略逃避先天性和适应性免疫反应的清除,其中包括对效应免疫细胞的主动抑制。调节性T淋巴细胞(Treg)和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至关重要的作用。暴露于肿瘤衍生因子的分化树突状细胞(DC)可能停滞在未成熟阶段,无法启动免疫反应,并可能诱导效应T细胞无反应或缺失。这些在不同类型癌症患者中积累的耐受性DC也参与了Treg的产生。反过来,在肿瘤进展过程中扩增的Treg通过阻碍DC协调免疫反应的能力和直接抑制抗肿瘤T淋巴细胞,促进癌症的免疫耐受。在此,我们综述DC和Treg之间与促进癌症诱导的耐受性相关的双向通讯。