Institute for Molecular Bioscience, and Centre for Inflammation and Disease Research, The University of Queensland, St. Lucia, Australia.
Quench Bio, Inc., Cambridge, MA, USA.
Methods Mol Biol. 2023;2696:199-210. doi: 10.1007/978-1-0716-3350-2_13.
The Nod-like Receptor (NLR) apoptosis inhibitory proteins (NAIPs) are cytosolic receptors that sense cytosolic bacterial proteins. NAIP ligation induces its association with NLRC4, leading to the assembly of the NAIP/NLRC4 inflammasome, which induces the activation of the caspase-1 protease. Caspase-1 then cleaves pro-interleukin (IL)-1β, pro-IL-18, and gasdermin D and induces a form of pro-inflammatory cell death, pyroptosis. These processes culminate in host defense against bacterial infection. Here we describe methods for activating NAIP/NLRC4 inflammasome signalling in human and murine macrophages and quantifying inflammasome-induced cell death.
核苷酸结合寡聚化结构域样受体（NLR）凋亡抑制蛋白（NAIP）是细胞溶质受体，可感知细胞溶质中的细菌蛋白。NAIP 连接诱导其与 NLRC4 结合，导致 NAIP/NLRC4 炎性小体的组装，从而诱导半胱天冬酶-1 蛋白酶的激活。然后，半胱天冬酶-1 切割前白细胞介素 (IL)-1β、前白细胞介素-18 和 gasdermin D，并诱导一种促炎细胞死亡形式，即细胞焦亡。这些过程最终导致宿主对细菌感染的防御。在这里，我们描述了在人源和鼠源巨噬细胞中激活 NAIP/NLRC4 炎性小体信号转导并量化炎性小体诱导的细胞死亡的方法。
