Abstract
Inflammasomes are multimeric protein complexes that are formed in a cell to orchestrate host defense mechanisms against infectious agents and physiological aberration. Assembly of the inflammasome complex is initiated by nucleotide‐binding domain and leucine‐rich repeat receptors (NLRs) or absent in melanoma 2 (AIM2)‐like receptors (ALRs). NLRs and ALRs mediate host recognition of pathogen‐associated molecular patterns (PAMPs) released during bacterial, viral, fungal, and protozoan infections, or danger‐associated molecular patterns (DAMPs) released during cellular damage. Activated NLRs and ALRs, in most cases, recruit a bipartite protein known as ASC to engage caspase‐1. NLR‐ and ALR‐mediated caspase‐1 activation drives pyroptosis and are largely beneficial to the host during an infection. However, these cytokines induced by endogenous danger signals trigger sterile inflammation, a risk factor for the development of autoinflammatory and metabolic diseases. Therefore, activation of the inflammasome must be finely controlled to avoid overt tissue damage. These regulatory activities are governed by scaffolding proteins and post‐translational modifications, which together, tightly control and modulate inflammasome activation.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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