CLEC4D

Chr 12

C-type lectin domain family 4 member D

Also known as: CD368, CLEC-6, CLEC6, CLECSF8, Dectin-3, MCL, MPCL

The protein functions as a calcium-dependent pattern recognition receptor in the innate immune system, recognizing pathogen-associated molecular patterns from bacteria and fungi to activate immune responses through NF-kappa-B signaling. Biallelic mutations in this gene cause a primary immunodeficiency disorder characterized by recurrent invasive fungal infections, particularly severe candidiasis. The gene shows very low constraint against loss-of-function variants (pLI near 0), and the condition follows an autosomal recessive inheritance pattern.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
20
Pubs (1 yr)
39
P/LP submissions
0%
P/LP missense
1.57
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryCLEC4D
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
38 unique Pathogenic / Likely Pathogenic· 39 VUS of 88 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.57LOEUF
pLI 0.000
Z-score 0.25
OE 0.91 (0.551.57)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-0.12Z-score
OE missense 1.03 (0.891.20)
120 obs / 116.5 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE0.91 (0.551.57)
00.351.4
Missense OE1.03 (0.891.20)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 9 / 9.9Missense obs/exp: 120 / 116.5Syn Z: 0.09
DN
0.7131th %ile
GOF
0.7029th %ile
LOF
0.2776th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

88 submitted variants in ClinVar

Classification Summary

Pathogenic36
Likely Pathogenic2
VUS39
Likely Benign5
Benign1
36
Pathogenic
2
Likely Pathogenic
39
VUS
5
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
36
0
36
Likely Pathogenic
0
0
2
0
2
VUS
0
34
5
0
39
Likely Benign
0
3
1
1
5
Benign
0
1
0
0
1
Total03844183

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

CLEC4D · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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