Structural, expression, and evolutionary analysis of mouse CIAS1

Anderson, Justin P.; Mueller, James L.; Rosengren, Sanna; Boyle, David L.; Schaner, Philip E.; Cannon, Steven B.; Goodyear, Carl S.; Hoffman, Hal M.

doi:10.1016/j.gene.2004.05.002

Cited by 49 publications

(46 citation statements)

References 38 publications

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“…This is in contrast to Northern blot analysis of human tissues where NALP3 expression was found to be restricted to peripheral blood leukocytes . Anderson et al (2004) recently examined the expression of NALP3 in mouse tissues by quantitative real-time PCR, and they also noted NALP3 expression in a wide variety of tissues, with particularly high expression in the skin and eye. We also detected NALP3 mRNA by RT-PCR and SYBR green quantitative RT-PCR analysis in various primary immune cells (Figures 1B and 1C).…”

Section: Expression Of Nalp3mentioning

confidence: 99%

Critical Role for NALP3/CIAS1/Cryopyrin in Innate and Adaptive Immunity through Its Regulation of Caspase-1

et al. 2006

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Mutations in the NALP3/CIAS1/cryopyrin gene are linked to three autoinflammatory disorders: Muckle-Wells syndrome, familial cold autoinflammatory syndrome, and chronic infantile neurologic cutaneous and articular syndrome. NALP3, with the adaptor molecule ASC, has been proposed to form a caspase-1-activating "inflammasome," a complex with pro-IL1beta-processing activity. Here, we demonstrate the effect of NALP3 deficiency on caspase-1 function. NALP3 was essential for the ATP-driven activation of caspase-1 in lipopolysaccharide-stimulated macrophages and for the efficient secretion of the caspase-1-dependent cytokines IL-1alpha, IL-1beta, and IL-18. IL-1beta has been shown to play a key role in contact hypersensitivity; we show that ASC- and NALP3-deficient mice also demonstrate an impaired contact hypersensitivity response to the hapten trinitrophenylchloride. NALP3, however, was not required for caspase-1 activation by Salmonella typhimurium, and NALP3 deficiency only partially protects mice from the lethal effects of endotoxin. These data suggest that NALP3 plays a specific role in the caspase-1 activation pathway.

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Section: Expression Of Nalp3mentioning

confidence: 99%

Critical Role for NALP3/CIAS1/Cryopyrin in Innate and Adaptive Immunity through Its Regulation of Caspase-1

et al. 2006

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“…Some genetic variations (such as V198M) have been identified in normal patients or in patients with undefined or other inflammatory diseases, suggesting that NLRP3 variations may play a role in more common diseases, such as rheumatoid arthritis, systemic lupus erythematosus, or gout. The NLRP3 gene is highly conserved throughout mammalian evolution, suggesting purifying selection [33].…”

Section: Geneticsmentioning

confidence: 99%

Hereditary immunologic disorders caused by pyrin and cryopyrin

Hoffman

2007

Curr Allergy Asthma Rep

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A new family of hereditary immunologic disorders known as the autoinflammatory diseases involves dysregulation of the innate immune system. Elucidation of the genetic basis of these disorders has resulted in improved understanding of the disease pathophysiology of systemic and tissue inflammation, and has also revealed novel nonpathologic innate immune mechanisms. These advances have also resulted in direct improvement in diagnosis and therapy for autoinflammatory disorders such as the cryopyrinopathies and familial Mediterranean fever and have implications for more common inflammatory diseases.

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“…Autoinflammatory diseases (Anderson et al, 2004) are clinical disorders marked by abnormally increased inflammation, mediated predominantly by the cells and molecules of the innate immune system (Kastner et al, 2010). Familial Mediterranean fever (FMF) is the most common autoinflammatory disease all over the world.…”

Section: Introductionmentioning

confidence: 99%