Gene2 diseases

NLRP3

8 variant(s) documented across Schnitzler Syndrome, Cryopyrin-Associated Periodic Syndromes

Found across diseases

Variants

VariantTypeFrequency in diseaseSignificanceAlso found in
Somatic mosaicism (various)somaticRare (2 confirmed cases)Found in patients with the most severe phenotypes. Demonstrates that NLRP3 can be directly causative in some cases.CAPS (Nearly all cases (germline))
V198Mgermline1 family studiedFound in 1 patient but 4 asymptomatic carriers across 3 generations — insufficient alone to cause disease.CAPS (mild forms) (Occasional)
Multiple pathogenic variants (>250)germline~50-70% detectable by SangerGain-of-function mutations causing constitutive inflammasome activation. Most in exon 3 (NACHT domain).Schnitzler syndrome (somatic mosaicism, rare) (Rare); Gout (common variants) (Common)
R260WgermlineCommon MWS variantMost frequent MWS-associated variant in French population.
T348MgermlineCommon in severe CAPSAssociated with early onset, chronic course, hearing loss.
Somatic mosaicism variantssomatic40% of mutation-negative CAPSLow-level allele frequency (1.9–45%); can increase over time. Explains 'mutation-negative' CAPS.Schnitzler syndrome (Rare)
De novo mutationsgermline~50-60% of NOMIDSpontaneous new mutations; no family history.
Y861 LRR domain variantsgermlineRareAtypical phenotype with minimal cold-triggered rash.

Clinical implications

Somatic mosaicism (various)

Supports inflammasome-driven model. Does not currently change treatment approach.

Testing: deep sequencing, mosaicism-specific assays

V198M

Low-penetrance variant. Not diagnostic on its own.

Testing: Sanger sequencing

Multiple pathogenic variants (>250)

Confirms CAPS diagnosis; genotype-phenotype correlation guides prognosis (certain variants → more severe disease).

Testing: Sanger sequencing, targeted gene panels, WES

R260W

Typical MWS phenotype with hearing loss risk.

Testing: Sanger sequencing

T348M

Higher risk of neurological involvement; may require higher dose IL-1 blockade.

Testing: Sanger sequencing

Somatic mosaicism variants

Deep sequencing required for detection; can cause late adult-onset disease.

Testing: Amplicon-based deep sequencing, massively parallel sequencing

De novo mutations

Most NOMID cases are sporadic; genetic counseling important.

Testing: Sanger sequencing, WES

Y861 LRR domain variants

Non-classical presentation; may be missed by clinical criteria alone.

Testing: Sanger sequencing

Related molecules in pathway

NLRP3strong

Inflammasome sensorDysregulated

Related hypotheses

NLRP3 somatic mosaicism is the primary driver in a subset of patients

20
emerging·8 studies

Pyrin-inflammasome dysfunction (MEFV variants) contributes to pathogenesis

15
emerging·4 studies

Sources (10)

C1de Koning HD et al. (2015) NLRP3 somatic mosaicism in variant SchnitzlerDOI
C2Aksentijevich I et al. (2002) De novo CIAS1 mutations, cytokine activation, and evidence for genetic heterogeneity in patients with NOMIDPubMed
A1Hoffman HM et al. (2001) Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndromePubMed
B4Booshehri LM et al. (2019) CAPS and NLRP3PubMed
J7Cuisset L et al. (2011) Mutations in the autoinflammatory cryopyrin-associated periodic syndrome gene: epidemiological study and lessons from eight years of genetic analysis in FrancePubMed
A4Levy R et al. (2015) Phenotypic and genotypic characteristics of CAPS: a series of 136 patients from the Eurofever RegistryPubMed
C3Tanaka N et al. (2011) High incidence of NLRP3 somatic mosaicism in patients with chronic infantile neurologic, cutaneous, articular syndromePubMed
C4Rowczenio DM et al. (2017) Late-onset cryopyrin-associated periodic syndromes caused by somatic NLRP3 mosaicism — UK single center experiencePubMed
C5Izawa K et al. (2012) Detection of base substitution-type somatic mosaicism of the NLRP3 gene with >99.9% statistical confidence by massively parallel sequencingPubMed
C7Melo Gomes S et al. (2025) Somatic NLRP3 mosaicism in patients with 'mutation-negative' CAPS: insights from a single centre UK cohort