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2015 ; 265
(1
): 6-21
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Regulation of inflammasome activation
#MMPMID25879280
Man SM
; Kanneganti TD
Immunol Rev
2015[May]; 265
(1
): 6-21
PMID25879280
show ga
Inflammasome biology is one of the most exciting and rapidly growing areas in
immunology. Over the past 10 years, inflammasomes have been recognized for their
roles in the host defense against invading pathogens and in the development of
cancer, auto-inflammatory, metabolic, and neurodegenerative diseases. Assembly of
an inflammasome complex requires cytosolic sensing of pathogen-associated
molecular patterns or danger-associated molecular patterns by a
nucleotide-binding domain and leucine-rich repeat receptor (NLR) or absent in
melanoma 2 (AIM2)-like receptors (ALR). NLRs and ALRs engage caspase-1, in most
cases requiring the adapter protein apoptosis-associated speck-like protein
containing a CARD (ASC), to catalyze proteolytic cleavage of pro-interleukin-1?
(pro-IL-1?) and pro-IL-18 and drive pyroptosis. Recent studies indicate that
caspase-8, caspase-11, IL-1R-associated kinases (IRAK), and receptor-interacting
protein (RIP) kinases contribute to inflammasome functions. In addition,
post-translational modifications, including ubiquitination, deubiquitination,
phosphorylation, and degradation control almost every aspect of inflammasome
activities. Genetic studies indicate that mutations in NLRP1, NLRP3, NLRC4, and
AIM2 are linked with the development of auto-inflammatory diseases,
enterocolitis, and cancer. Overall, these findings transform our understanding of
the basic biology and clinical relevance of inflammasomes. In this review, we
provide an overview of the latest development of inflammasome research and
discuss how inflammasome activities govern health and disease.
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