Delinking CARD9 and IL-17: CARD9 Protects againstCandida tropicalisInfection through a TNF-α–Dependent, IL-17–Independent Mechanism

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Delinking CARD9 and IL-17: CARD9 Protects against Candida tropicalis Infection through a TNF-α–Dependent, IL-17–Independent Mechanism

Candida is the third most common cause of bloodstream infections in hospitalized patients. Immunity to C. albicans, the most frequent species to be isolated in candidiasis, involves a well-characterized Dectin-1/caspase-associated recruitment domain adaptor 9 (CARD9)/IL-17 signaling axis. Infections caused by non-albicans Candida species are on the rise, but surprisingly little is known about i...

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Inflammatory bowel diseases (IBD) are key risk factors for the development of colorectal cancer, but the mechanisms that link intestinal inflammation with carcinogenesis are insufficiently understood. Card9 is a myeloid cell-specific signaling protein that regulates inflammatory responses downstream of various pattern recognition receptors and which cooperates with the inflammasomes for IL-1β p...

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CARD9 gene silencing with siRNA protects rats against severe acute pancreatitis: CARD9‐dependent NF‐κB and P38MAPKs pathway

We previously reported the up-regulation of caspase recruitment domain 9 (CARD9) expressions in severe acute pancreatitis (SAP) patients, but little is known about its regulation. In this study, small interfering RNA (siRNA) was used to reduce the levels of CARD9 expression in sodium taurocholate-stimulated SAP rats. CARD9 was overexpressed in SAP rats, which correlated with the severity of pan...

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CARD9 negatively regulates NLRP3-induced IL-1β production on Salmonella infection of macrophages

Interleukin-1β (IL-1β) is a proinflammatory cytokine required for host control of bacterial infections, and its production must be tightly regulated to prevent excessive inflammation. Here we show that caspase recruitment domain-containing protein 9 (CARD9), a protein associated with induction of proinflammatory cytokines by fungi, has a negative role on IL-1β production during bacterial infect...

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ژورنال

عنوان ژورنال: The Journal of Immunology

سال: 2015

ISSN: 0022-1767,1550-6606

DOI: 10.4049/jimmunol.1500870