Molecular mechanisms of inflammasome signaling

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

Anukriti Mathur^1¹ 

[1] Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, Australian National University, Canberra, Australia^1

关键词: AIM2;    NLRP1/3;    NLRC4;    Pyrin;    caspases;   

DOI  :  10.1189/jlb.3MR0617-250R

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

The inflammasome is a macromolecular protein complex that mediates proteolytic cleavage of pro‐IL‐1β and ‐IL‐18 and induces cell death in the form of pyroptosis. Certain nucleotide‐binding oligomerization domain‐like receptors (NLRs), absent in melanoma 2 (AIM2)‐like receptors (ALRs), or tripartite motif (TRIM) family receptors trigger the assembly of an inflammasome in response to pathogen‐associated molecular patterns (PAMPs) or danger‐associated molecular patterns (DAMPs). Recent studies have revealed a multitude of host components and signals that are essential for controlling canonical and noncanonical inflammasome activation and pyroptosis. These include pore‐forming gasdermin proteins, the never in mitosis A‐related kinase 7 (NEK7), IFN‐inducible proteins (IFIs), reactive oxygen species (ROS), autophagy, potassium efflux, mitochondrial perturbations, and microbial metabolites. Here, we provide a comprehensive overview of the molecular and signaling mechanisms that provide stringent regulation over the activation and effector functions of the inflammasome.

【 授权许可】

CC BY