University of Massachusetts Medical School, Department of Infectious Diseases and Immunology, 364 Plantation St, Worcester, MA 01605, USA.
Curr Opin Immunol. 2010 Feb;22(1):28-33. doi: 10.1016/j.coi.2009.12.004. Epub 2010 Jan 8.
In response to injurious or infectious agents caspase-1 activating multiprotein complexes, termed inflammasomes, assemble in the cytoplasm of cells. Activated caspase-1 cleaves the proforms of the interleukin-1 cytokine family members leading to their activation and secretion. The IL-1 family cytokines have multiple proinflammatory activities implicating them in the pathogenesis of many inflammatory diseases. While defined ligands have been identified for the NLRP1, IPAF, and AIM2 inflammasomes, little is known about the activation mechanisms of the NLRP3 inflammasome. Numerous different molecular entities, such as various crystals, pore-forming toxins, or extracellular ATP can trigger the NLRP3 inflammasome. Recent work proposes that NLRP3 is activated indirectly by host factors that are generated in response to NLRP3 triggers.
针对伤害性或传染性因子，细胞浆中会组装称为炎性小体的半胱氨酸蛋白酶-1 激活多蛋白复合物。激活的半胱天冬酶-1 切割白细胞介素-1 细胞因子家族成员的前体形式，导致其激活和分泌。IL-1 家族细胞因子具有多种促炎活性，使其参与许多炎症性疾病的发病机制。虽然已经确定了 NLRP1、IPAF 和 AIM2 炎性小体的定义配体，但 NLRP3 炎性小体的激活机制知之甚少。许多不同的分子实体，如各种晶体、形成孔的毒素或细胞外 ATP，都可以触发 NLRP3 炎性小体。最近的研究提出，NLRP3 是通过宿主因子间接激活的，这些因子是对 NLRP3 触发的反应产生的。
