Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, USA.
Curr Opin Immunol. 2011 Oct;23(5):591-7. doi: 10.1016/j.coi.2011.07.005. Epub 2011 Aug 10.
The inflammasome-forming NLRs are well characterized members of a protein complex mediating the activation of caspase-1 and the cleavage of pro-IL-1β and pro-IL-18 into their active, secreted forms. New data suggest that components of the inflammasome cascade may have roles in influencing inflammasome-independent pathways of cytokine production. These influences on other immune cytokine pathways are complemented by data suggesting that non-inflammasome cytokines can influence the activation of the inflammasome, either directly or by influencing transcription of inflammasome components. The crosstalk between these cytokine cascades may lead to increased abilities for the cell to respond to diverse pathogen threats.
炎性小体形成的 NLR 是一种蛋白复合物的特征成员,该复合物介导半胱天冬酶-1 的激活以及前白细胞介素-1β和前白细胞介素-18 切割成其活性、分泌形式。新数据表明,炎性小体级联的成分可能在影响炎性小体非依赖性细胞因子产生途径方面发挥作用。这些对其他免疫细胞因子途径的影响,加上数据表明非炎性细胞因子可以直接影响炎性小体成分的转录,或者通过影响炎性小体成分的转录来影响炎性小体的激活。这些细胞因子级联之间的串扰可能导致细胞对各种病原体威胁的反应能力增强。