Department of Biochemistry, Ghent University, B-9000 Ghent, Belgium.
J Immunol. 2011 Jul 15;187(2):597-602. doi: 10.4049/jimmunol.1100229.
Inflammasomes are emerging as key regulators of the host response against microbial pathogens. These cytosolic multiprotein complexes recruit and activate the cysteine protease caspase-1 when microbes invade sterile tissues or elicit cellular damage. Inflammasome-activated caspase-1 induces inflammation by cleaving the proinflammatory cytokines IL-1β and IL-18 into their biologically active forms and by releasing the alarmin HMGB1 into the extracellular milieu. Additionally, inflammasomes counter bacterial replication and clear infected immune cells through an inflammatory cell death program termed pyroptosis. As a countermeasure, bacterial and viral pathogens evolved virulence factors to antagonize inflammasome pathways. In this review, we discuss recent progress on how inflammasomes contribute to host defense against bacterial and viral pathogens, and we review how viruses and bacteria modulate inflammasome function to their benefit.
炎症小体作为宿主对抗微生物病原体反应的关键调节剂而出现。当微生物侵入无菌组织或引起细胞损伤时,这些细胞溶质多蛋白复合物募集并激活半胱氨酸蛋白酶 caspase-1。炎症小体激活的 caspase-1 通过将促炎细胞因子 IL-1β 和 IL-18 切割成其生物活性形式,并将警报素 HMGB1 释放到细胞外环境中,诱导炎症。此外,炎症小体通过一种称为细胞焦亡的炎症性细胞死亡程序来抑制细菌复制和清除感染的免疫细胞。作为一种对策,细菌和病毒病原体进化出了毒力因子来拮抗炎症小体途径。在这篇综述中,我们讨论了炎症小体如何有助于宿主防御细菌和病毒病原体的最新进展,并回顾了病毒和细菌如何调节炎症小体功能以利于自身。