The role of the NLRP3 inflammasome in regulation of antiviral responses to influenza A virus infection.

摘要: The innate immune system provides the host with both a dynamic barrier to prevent infection and means which rapid anti-microbial responses can be mounted. inflammasome pathway is critical early response mechanism that enables detection of pathogens initiates production inflammatory cytokines, inducing recruitment effector cells site infection. complete activation requires two signals: an initial priming step upon pathogen, followed by intracellular pattern recognition receptors formation complex. complex made multiprotein oligomers includes sensor protein such as nucleotide-binding oligomerization domain (NOD) like receptor proteins (NLRP), adapter protein, ASC, critically activates pro-caspase-1. mature caspase-1 then proteolytically cleaves cytosolic pro-IL-1β pro-IL-18, are secreted cytokines activate arm Active also results in pyroptosis, form cell death triggered inflammation. induction IL-1β IL-18 considered signatures for activation. With focus influenza A virus infection, this review will address present knowledge on mechanisms activation, particularly how viral components modulate NOD-like protein-3 (NLRP3)-dependent We discuss potential therapeutic strategies target ameliorate illness, well novel methods vaccination stimulation aim increase efficacy.