Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation: genes and variants

Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation is linked to 1 analyzed protein (PLCG2). 3 DNA variants are known to cause it; 93 more are uncertain, and 0 of those already look disease-causing on computable evidence.

Last updated 2026-09-30. Research information, not medical advice.

Genes linked to Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation

Known disease-causing variants in Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation

VariantPositionProtein partClinical label
PLCG2 S707Y707SH2 2Disease-causing
PLCG2 S707P707SH2 2Disease-causing
PLCG2 L845S845Disease-causing

Same protein, different disease

Diseases related to Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation

Frequently asked questions

Which genes are linked to Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation?

In CATVariant, Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation is linked to 1 analyzed protein: PLCG2 (1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-2).

How many genetic variants are linked to Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation?

103 variants: 3 are classified as disease-causing (pathogenic or likely pathogenic) in ClinVar and 93 are of uncertain significance or have conflicting reports.

Which uncertain variants in Autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation look disease-causing?

None of the uncertain variants currently reaches the likely-pathogenic range on computable evidence alone.

About this data

Variant–disease links come from ClinVar, Open Targets and UniProt, pooled from the latest public CATVariant analysis of each human protein. Evidence scores use the ACMG/AMP Bayesian points scale with computable criteria only (position among known disease variants, rarity in gnomAD, calibrated predictors, deep mutational scanning); there is no family or patient data, so they prioritise variants for expert review and never classify them.

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