摘要

Interleukin (IL)-32 is a newly described proinflammatory cytokine that seems likely to play a role in inflammation and host defense. Little is known about the regulation of IL-32 production by primary cells of the immune system.In the present study, freshly obtained human peripheral blood mononuclear cells were stimulated with different Toll-like receptor (TLR) agonists, and gene expression and synthesis of IL-32 was determined. We demonstrate that the TLR4 agonist lipopolysaccharide induces moderate (4-fold) production of IL-32, whereas agonists of TLR2, TLR3, TLR5, or TLR9, each of which strongly induced tumor necrosis factor alpha and IL-6, did not stimulate IL-32 production. However, the greatest amount of IL-32 was induced by the mycobacteria Mycobacterium tuberculosis and M. bovis BCG (20-fold over unstimulated cells). IL-32-induced synthesis by either lipopolysaccharide or mycobacteria remains entirely cell-associated in monocytes; moreover, steady-state mRNA levels are present in unstimulated monocytes without translation into IL-32 protein, similar to other cytokines lacking a signal peptide. IL-32 production induced by M. tuberculosis is dependent on endogenous interferon-gamma (IFNgamma); endogenous IFNgamma is, in turn, dependent on M. tuberculosis-induced IL-18 via caspase-1.In conclusion, IL-32 is a cell-associated proinflammatory cytokine, which is specifically stimulated by mycobacteria through a caspase-1- and IL-18-dependent production of IFNgamma.

译文

白细胞介素 (IL)-32 是一种新描述的促炎细胞因子,似乎可能在炎症和宿主防御中发挥作用。关于免疫系统初级细胞对 IL-32 产生的调节知之甚少。在本研究中,用不同的 Toll 样受体 (TLR) 激动剂刺激新获得的人外周血单个核细胞,并测定 IL-32 的基因表达和合成。我们证明了 TLR4 激动剂脂多糖诱导适度 (4 倍) 产生 IL-32,而 TLR2 、 TLR3 、 TLR5 或 TLR9 激动剂, 其中每一个都强烈诱导肿瘤坏死因子 α 和 IL-6,没有刺激 IL-32 的产生。然而,最大的 IL-32 量是由结核分枝杆菌和牛分枝杆菌 BCG (20 倍于未刺激细胞) 诱导的。由脂多糖或分枝杆菌合成的 IL-32-induced 在单核细胞中仍然完全与细胞相关; 此外,稳定状态的 mRNA 水平存在于未刺激的单核细胞中,而没有转化为 IL-32 的蛋白质, 与其他缺少信号肽的细胞因子相似。M 诱导的 IL-32 产生。结核病依赖于内源性 γ 干扰素 (IFNgamma); 内源性 γ 干扰素反过来依赖于 M。结核病诱导的 IL-18 通过 caspase-1.In 的结论,IL-32 是一种细胞相关的促炎细胞因子,它是通过一种 caspase-1 和 IL-18-dependent 的 IFNgamma 的产生被分枝杆菌特异性刺激的。

Caspase

神经 临床研究术语
概述  :  

也称半胱天冬酶,细胞凋亡蛋白酶分为启动型和执行型,前者接受死亡信号、启动凋亡或激活下游的分子,后者则降解细胞骨架、蛋白质、核酸等。半胱天冬酶如何启动和实施凋亡、受哪些因素调节等问题是近年来生命科学研究领域的热点之一。两条激活途径细胞外途径:胞外配体与胞膜受体结合后,衔接蛋白作为一个平台,提供场所给上游前半胱天冬酶-8完成聚合及相互剪切之用。前半胱大冬酶-8与受体蛋白结合后,同受体一起形成凋亡体,前半胱天冬酶间的聚合需要依赖其前区的两种特殊结构:DED区和CARD区。细胞内途径:细胞凋亡启动后

caspase

释    义   n. 半胱天冬酶;切冬酶(胱冬肽酶);细胞凋亡蛋白酶

例    句   The inflammasomes join together and activate a protein, caspase-1, that in turn triggers an inflammatory response.  这些炎症小体联合起来可以激活半胱天冬酶-1,这种蛋白依次激活炎症的级联反应。

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