论文部分内容阅读
炎症小体是由细胞内核苷酸结合寡聚化结构域(NOD)样受体介导组装的胞质复合物,它们启动天然免疫识别病原菌和危险信号后,激活caspase-1,进而导致白细胞介素(IL-1β和IL-18)等炎症因子成熟及分泌一种称为“pyrotosis”的特殊细胞死亡。最近发现一个新的非经典炎性小体可激活caspase-11,它是一种在脂多糖诱导致死性中所需的促炎性caspase。该研究还强调指出,先前生成的caspase-1基因敲除小鼠缺乏功能性等位基因的Casp11(也称CASP4),使小鼠Casp1和Casp11双敲除。以往研究表明,这些老鼠更易
Inflammasomes are cytoplasmic complexes that are assembled by intracellular nucleotide-binding oligomerization domain (NOD) -like receptors that activate caspase-1 upon initiation of innate immunity-identifying pathogens and danger signals, leading to leukocyte-mediated Inflammatory cytokines such as IL-1β and IL-18 mature and secrete a specific cell death called “pyrotosis”. A new, non-classical inflammasome has recently been found to activate caspase-11, a proinflammatory caspase required for lipopolysaccharide-induced lethality. The study also underlines the fact that previously-generated caspase-1 knockout mice lacked the functional allele of Casp11 (also known as CASP4) and double knocked out Casp1 and Casp11 in mice. Previous studies have shown that these mice are easier