Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
Science. 2012 Apr 27;336(6080):481-5. doi: 10.1126/science.1217141. Epub 2012 Mar 29.
Inflammasomes are sensory complexes that alert the immune system to the presence of infection or tissue damage. These complexes assemble NLR (nucleotide binding and oligomerization, leucine-rich repeat) or ALR (absent in melanoma 2-like receptor) proteins to activate caspase-1 cleavage and interleukin (IL)-1β/IL-18 secretion. Here, we identified a non-NLR/ALR human protein that stimulates inflammasome assembly: guanylate binding protein 5 (GBP5). GBP5 promoted selective NLRP3 inflammasome responses to pathogenic bacteria and soluble but not crystalline inflammasome priming agents. Generation of Gbp5(-/-) mice revealed pronounced caspase-1 and IL-1β/IL-18 cleavage defects in vitro and impaired host defense and Nlrp3-dependent inflammatory responses in vivo. Thus, GBP5 serves as a unique rheostat for NLRP3 inflammasome activation and extends our understanding of the inflammasome complex beyond its core machinery.
炎性小体是一种感知复合物,可向免疫系统发出感染或组织损伤的信号。这些复合物组装 NOD(核苷酸结合寡聚化结构域)样受体(NLR)或黑色素瘤缺失 2 样受体(ALR)蛋白,以激活半胱氨酸蛋白酶-1 的切割和白细胞介素(IL)-1β/IL-18 的分泌。在这里,我们鉴定了一种非 NLR/ALR 人蛋白,可刺激炎性小体组装:鸟苷酸结合蛋白 5(GBP5)。GBP5 促进对致病性细菌和可溶性但非结晶性炎性小体引发剂的选择性 NLRP3 炎性小体反应。生成 Gbp5(-/-) 小鼠显示体外 caspase-1 和 IL-1β/IL-18 切割缺陷,以及体内宿主防御和 Nlrp3 依赖性炎症反应受损。因此,GBP5 作为 NLRP3 炎性小体激活的独特变阻器,扩展了我们对炎性小体复合物的理解,超越了其核心机制。