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Journal ArticleDOI

Host inflammatory responses to intracellular invaders: Review study

TLDR
Inflammasome components assemble and oligomerizes leading to the auto cleavage of the pro-caspase-1 to its active form and controls the establishment of the pathogen by mounting inflammatory response and activation of the pyroptotic cell death.
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This article is published in Life Sciences.The article was published on 2020-01-01. It has received 18 citations till now. The article focuses on the topics: Pyroptosis & Inflammasome.

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Citations
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Journal ArticleDOI

NLRP3 Inflammasome and Inflammatory Diseases.

TL;DR: In this review, NLRP3 regulation and activation, its proinflammatory role ininflammatory diseases, interactions with autophagy, and targeted therapeutic approaches in inflammatory diseases will be summarized.
Journal ArticleDOI

Nootkatone Inhibits Acute and Chronic Inflammatory Responses in Mice.

TL;DR: NTK exerted anti-inflammatory effects that are associated with inhibition of IL1-β and TNF-α production, possibly due to inhibition of COX-2 activity and antagonism of the H1 receptor, but further studies are required to characterize the effects of this compound on chronic inflammation.
Journal ArticleDOI

Toll-like receptor 3 (TLR3) regulation mechanisms and roles in antiviral innate immune responses.

TL;DR: In this article, the authors focus on recent advances in understanding the antiviral mechanism of the TRIF pathway and describe the essential characteristics of TLR3 and its antiviral effects, which may contribute to disease diagnosis and could foster the development of novel treatments for viral diseases.
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Ion Efflux and Influenza Infection Trigger NLRP3 Inflammasome Signaling in Human Dendritic Cells

TL;DR: In this article, the authors delineate the contribution of the NLRP3 inflammasome to the secretion of IL-1β, IL-18, and IL 1α by human Dendritic cells (MDDCs) and primary conventional (cDCs).
References
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Journal ArticleDOI

Innate Immune Recognition

TL;DR: Microbial recognition by Toll-like receptors helps to direct adaptive immune responses to antigens derived from microbial pathogens to distinguish infectious nonself from noninfectious self.
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The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta.

TL;DR: In this article, the inflammasome is identified as a caspase-activating complex that comprises caspases-1, casp-5, Pycard/Asc, and NALP1, a Pyrin domain-containing protein sharing structural homology with NODs.
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Origin and Physiological Roles of Inflammation

TL;DR: This work has shown that tissue stress or malfunction induces an adaptive response that is intermediate between the basal homeostatic state and a classic inflammatory response, which is referred to here as para-inflammation.
Journal ArticleDOI

Gout-associated uric acid crystals activate the NALP3 inflammasome

TL;DR: It is shown that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18 in mice deficient in the IL-1β receptor.
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The peroxisome proliferator-activated receptor-gamma is a negative regulator of macrophage activation

TL;DR: It is shown that PPAR-γ is markedly upregulated in activated macrophages and inhibits the expression of the inducible nitric oxide synthase, gelatinase B and scavenger receptor A genes in response to 15d-PGJ2 and synthetic PPar-γ ligands, suggesting that PPARS and locally produced prostaglandin D2 metabolites are involved in the regulation of inflammatory responses.
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