Sensing and Reacting to Microbes via the Inflammasomes

Sensing and Reacting to Microbes via the Inflammasomes

2012 September 23 | Luigi Franchi, Raul Muñoz-Planillo, and Gabriel Núñez
Inflammasomes are multi-protein complexes that activate Caspase-1, leading to the maturation of proinflammatory cytokines IL-1β and IL-18 and the induction of pyroptosis. Members of the Nod-like receptor (NLR) family, such as NLRP1, Nlrp3, Nlr4, and AIM2, are critical components of inflammasomes, linking microbial and endogenous danger signals to Caspase-1 activation. In response to microbial infection, inflammasome activation contributes to host protection by inducing immune responses that limit microbial invasion. However, deregulated activation of inflammasomes is associated with autoinflammatory syndromes and other pathologies. Understanding inflammasome pathways provides insights into host defense against microbes and the development of inflammatory disorders. The review focuses on the activation, regulation, and function of NLR inflammasomes, emphasizing their interaction with microbes and their role in host defense.Inflammasomes are multi-protein complexes that activate Caspase-1, leading to the maturation of proinflammatory cytokines IL-1β and IL-18 and the induction of pyroptosis. Members of the Nod-like receptor (NLR) family, such as NLRP1, Nlrp3, Nlr4, and AIM2, are critical components of inflammasomes, linking microbial and endogenous danger signals to Caspase-1 activation. In response to microbial infection, inflammasome activation contributes to host protection by inducing immune responses that limit microbial invasion. However, deregulated activation of inflammasomes is associated with autoinflammatory syndromes and other pathologies. Understanding inflammasome pathways provides insights into host defense against microbes and the development of inflammatory disorders. The review focuses on the activation, regulation, and function of NLR inflammasomes, emphasizing their interaction with microbes and their role in host defense.
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