CLEC5A is critical for dengue virus–induced inflammasome activation in human macrophages

TL;DR: Investigation of interleukin (IL)-1β synthesis, processing, and secretion in platelets during dengue virus (DV) infection and potential contribution of these events to endothelial permeability during infection finds that platelets contribute to increased vascular permeability in DV infection by inflammasome-dependent release of IL-1β.

TL;DR: The currently available knowledge regarding the flavivirus receptors described so far is presented with specific attention to C-type lectin receptors and the phosphatidylserine receptors, T-cell immunoglobulin and mucin domain and TYRO3, AXL and MER (TAM).

TL;DR: The induction of multiple pathways of cellDeath has probably evolved to counteract microbial evasion of cell death pathways.

TL;DR: It is reported that exogenous IL-1β induces interferon regulatory factor 3 (IRF3) activation in human myeloid, fibroblast, and epithelial cells, with important implications for cGAS-STING in integrating inflammatory and microbial cues for host defense.

TL;DR: It is demonstrated that silica and aluminum salt crystals activated inflammasomes formed by the cytoplasmic receptor NALP3, which senses lysosomal damage as an endogenous 'danger' signal.

TL;DR: The cellular sources of these cytokines, receptor signaling pathways, and induced markers and gene signatures are reviewed and the concept of macrophage activation in the context of the immune response is revisit.

TL;DR: It is shown that cell priming through multiple signaling receptors induces NLRP3 expression, which is identified to be a critical checkpoint for NLRP2 activation and signals provided by NF-κB activators are necessary but not sufficient forNLRP3 activation.

TL;DR: It is shown that asbestos and silica are sensed by the Nalp3 inflammasome, whose subsequent activation leads to interleukin-1β secretion, and support its role as a major proinflammatory “danger” receptor in particulate matter–related pulmonary diseases.