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Article

Gain-of-function Pyrin mutations induce NLRP3 protein-independent interleukin-1β activation and severe autoinflammation in mice.

Immunity - 27 May 2011

Chae Jae Jin, Cho Young-Hun, Lee Geun-Shik, Cheng Jun, Liu P Paul, Feigenbaum Lionel, Katz Stephen I, Kastner Daniel L

Abstract excerpt

Missense mutations in the C-terminal B30.2 domain of pyrin cause familial Mediterranean fever (FMF), the most common Mendelian autoinflammatory disease. However, it remains controversial as to whether FMF is due to the loss of an inhibitor of inflammation or to the activity of a proinflammatory molecule. We generated both pyrin-deficient mice and "knockin" mice harboring mutant human B30.2 domains. Homozygous...

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Source

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Identifiers

PMID: 21600797
DOI: 10.1016/j.immuni.2011.02.020
PMCID: PMC3129608

Genes

NLRP3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Gain-of-function Pyrin mutations induce NLRP3 protein-independent interleukin-1β activation and severe autoinflammation in mice.PMID 21600797Read ↗

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