Journal
MOLECULAR ASPECTS OF MEDICINE
Volume 76, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.mam.2020.100863
Keywords
Inflammasome; NAIP; NLRC4; Caspase; bacterial infection
Funding
- OHSU
- Kenneth Rainin foundation
- MRF
- Immunity in Cancer & Allergy PhD program of the University of Salzburg
- Marshall plan foundation
- Austrian Science Fund (FWF) [W1213] Funding Source: Austrian Science Fund (FWF)
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In this review we give an overview of the NAIP/NLRC4 activation mechanism as well as the described roles of this inflammasome, with a focus on in vivo infection and pathology. After ligand recognition by NAIP sensor proteins the NAIP/NLRC4 inflammasome forms through oligomerization with the NLRC4 adaptor to activate Caspase-1. The activating ligands are intracellular bacterial flagellin or type-3 secretion system components, delivered by pathogens. In vivo experiments indicate a role in macrophages during lung, spleen and liver infection and systemic sepsis like conditions, as well as in intestinal epithelial cells. Upon NAIP/NLRC4 activation in the intestine, epithelial cell extrusion is triggered in addition to the canonical inflammasome outcomes of cytokine cleavage and pyroptosis. Human patients with auto-activating mutations in NLRC4 present with an autoinflammatory syndrome including enterocolitis. Although one of the better understood inflammasomes in terms of mechanism, tissue specific functions of NAIP/NLRC4 are only beginning to be understood.
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