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Open AccessJournal ArticleDOI

A Yersinia Effector Protein Promotes Virulence by Preventing Inflammasome Recognition of the Type III Secretion System

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TLDR
It is demonstrated that caspase-1 activation in response to the Yersinia type III secretion system (T3SS) requires the adaptor ASC and involves both NLRP3 and NLRC4 inflammasomes, and a class of bacterial proteins interferes with cellular recognition of bacterial secretion systems and contributes to bacterial survival within host tissues.
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This article is published in Cell Host & Microbe.The article was published on 2010-05-20 and is currently open access. It has received 271 citations till now. The article focuses on the topics: Inflammasome & Type three secretion system.

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Journal ArticleDOI

The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases

TL;DR: Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge, and a review presents and integrates recent progress in the field.
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Sensing and reacting to microbes through the inflammasomes

TL;DR: Members of the Nod-like receptor (NLR) family, including NLRP1, NLRP3 and NLRC4, and the cytosolic receptor AIM2 are critical components of inflammasomes and link microbial and endogenous danger signals to the activation of caspase-1.
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Regulation of inflammasome signaling

TL;DR: The various regulatory mechanisms that have evolved to keep inflammasome signaling in check to maintain immunological balance are discussed.
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Regulation of inflammasome activation

TL;DR: Genetic studies indicate that mutations in NLRP1, NLRP3, NLRC4, and AIM2 are linked with the development of auto‐inflammatory diseases, enterocolitis, and cancer and transform the understanding of the basic biology and clinical relevance of inflammasomes.
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Pyroptotic cell death defends against intracellular pathogens

TL;DR: This review focuses on molecular and morphological characteristics of pyroptosis and the individual inflammasomes and their contribution to defense against infection in mice and humans.
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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Toll-like receptors: critical proteins linking innate and acquired immunity.

TL;DR: Evidence is accumulating that the signaling pathways associated with each TLR are not identical and may, therefore, result in different biological responses.
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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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Recognition of Commensal Microflora by Toll-Like Receptors Is Required for Intestinal Homeostasis

TL;DR: It is shown that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis and protection from injury.
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