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Interleukin 35

肿瘤

关键词肿瘤 临床研究术语 白细胞介素

词汇介绍

拓展阅读

解析

Interleukin   英 /ɪn'tə'lʊkɪn/   美 /ɪn'tə'lʊkɪn/

释    义   n. [生化] 白介素

例    句   To observe the effect of mizolastine on leukotriene B4(LTB4) and interleukin 5(IL 5) released by spleen lymphocytes of allergic mice challenged by ovalbumin(OVA). 观察咪唑斯汀对卵蛋白(OVA)致敏的小鼠脾淋巴细胞释放白三烯B4(LTB4)和白介素5(IL 5)的影响。

概述

白细胞介素35(Interleukin 3,IL-35)是由调节性T细胞产生的细胞因子,是IL-12家族中的一员,2007年首次在EB病毒感染的B细胞中发现,在免疫抑制中起作用。它是一个由IL-12α链和IL-27β链组成的二聚体蛋白,分别由两个独立的基因IL-12A和EBI3编码。调节性T细胞分泌产生的IL-35抑制免疫细胞的炎症应答。IL-35不在组织中持续表达,但是在炎性刺激物激活后,编码IL-35的基因由血管内皮细胞、平滑肌细胞和单核细胞转录。   小鼠的研究

Adaptive plasticity of IL-10+ and IL-35+ Treg cells cooperatively promotes tumor T cell exhaustion复制标题

IL-10 + 和IL-35 + Treg细胞的适应性可塑性协同促进肿瘤T细胞耗竭

发表时间:2019-04-01

影响因子:23.5

作者: Deepali V. Sawant

期刊:Nat. Immunol.

Regulatory T cells (Treg cells) maintain host self-tolerance but are a major barrier to effective cancer  immunotherapy. Treg cells subvert beneficial anti-tumor immunity by modulating inhibitory receptor expression on tumor-infiltrating lymphocytes (TILs); however, the underlying  mediators and mechanisms have remained elusive. Here, we found that the cytokines IL-10 and IL-35 (Ebi3-IL-12α  heterodimer) were divergently expressed by Treg cell subpopulations in the tumor microenvironment (TME) and cooperatively promoted  intratumoral T cell exhaustion by modulating several inhibitory receptor expression and exhaustion-associated transcriptomic signature of CD8+ TILs. While expression of BLIMP1 (encoded by Prdm1) was a common target, IL-10 and IL-35 differentially affected effector T cell versus memory T cell fates, respectively, highlighting their differential, partially overlapping but non-redundant regulation of anti-tumor immunity. Our results reveal previously unappreciated cooperative roles for Treg cell-derived IL-10 and IL-35 in promoting BLIMP1-dependent exhaustion of CD8+ TILs that limits effective anti-tumor immunity.

译文

调节性T细胞(Treg细胞)维持宿主的自我耐受性,但是有效癌症免疫治疗的主要障碍。Treg细胞通过调节肿瘤浸润淋巴细胞(til)上抑制性受体的表达来破坏有益的抗肿瘤免疫;然而,其潜在的介质和机制仍不清楚。在这里,我们发现细胞因子IL-10和IL-35(Ebi3-IL-12α异二聚体)在肿瘤微环境(TME)中由Treg细胞亚群分化表达,并通过调节CD8+til的几种抑制性受体表达和衰竭相关转录特征协同促进肿瘤内T细胞衰竭。BLIMP1(由Prdm1编码)的表达是一个共同的靶点,IL-10和IL-35分别影响效应T细胞和记忆T细胞的命运,突出了它们对抗肿瘤免疫的差异性、部分重叠但非冗余的调节。我们的研究结果揭示了先前未被重视的Treg细胞衍生IL-10和IL-35在促进CD8+TILs依赖的BLIMP1耗竭中的协同作用,这限制了有效的抗肿瘤免疫。