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Critical role for NALP3/CIAS1/Cryopyrin in innate and adaptive immunity through its regulation of caspase-1.

Abstract：

: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.

journal_name

Immunity

journal_title

Immunity

authors

Sutterwala FS,Ogura Y,Szczepanik M,Lara-Tejero M,Lichtenberger GS,Grant EP,Bertin J,Coyle AJ,Galán JE,Askenase PW,Flavell RA

doi

10.1016/j.immuni.2006.02.004

keywords:

subject

Has Abstract

pub_date

2006-03-01 00:00:00

pages

317-27

issue

3

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(06)00140-3

journal_volume

24

pub_type

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