ArticleThe Journal of allergy and clinical immunology2022
Novel role for caspase recruitment domain family member 14 and its genetic variant rs11652075 in skin filaggrin homeostasis.
Article in The Journal of allergy and clinical immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Massively parallel analysis of genotype-dependent enhancer activity among atopic dermatitis genetic risk variants.The Journal of allergy and clinical immunology · 2025Article
- Genome-wide cross-trait analysis of heterogeneous outcomes in early life atopic dermatitis.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2025Article
- Update on the genetics of allergic diseases.The Journal of allergy and clinical immunology · 2025Review
- MYC is in the CARDs: CBM complexes coordinate immune and MYC-dependent cellular function.Frontiers in molecular medicine · 2025Article
- Joint genotype and ancestry analysis identify novel loci associated with atopic dermatitis in African American population.HGG advances · 2024Article
- Bioinformatic analysis of molecular characteristics and oncogenic features of CARD14 in human cancer.Scientific reports · 2024Article
- Regulation of MYC by CARD14 in human epithelium is a determinant of epidermal homeostasis and disease.Cell reports · 2024Article
- Genetic and Immunological Pathogenesis of Atopic Dermatitis.The Journal of investigative dermatology · 2024Review
- Filaggrin loss-of-function variants are associated with atopic dermatitis phenotypes in a diverse, early-life prospective cohort.JCI insight · 2024Article
- Novel insights into atopic dermatitis.The Journal of allergy and clinical immunology · 2023Review
- Aberrant inflammasome activation as a driving force of human autoimmune skin disease.Frontiers in immunology · 2023Review
- Recent progress in the genetic and epigenetic underpinnings of atopy.The Journal of allergy and clinical immunology · 2023Review
- Cutaneous and Developmental Effects ofBiomedicines · 2022Article
- The role of the CBM complex in allergic inflammation and disease.The Journal of allergy and clinical immunology · 2022Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLow epidermal filaggrin (FLG) is a risk factor for atopic dermatitis (AD) and allergic comorbidity. FLG mutations do not fully explain the variation in epidermal FLG levels, highlighting that other genetic loci may also regulate FLG expression.
objectiveWe sought to identify genetic loci that regulate FLG expression and elucidate their functional and mechanistic consequences.
methodsA genome-wide association study of quantified skin FLG expression in lesional and baseline non(never)-lesional skin of children with AD in the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children cohort was conducted. Clustered regularly interspaced short palindromic repeat approaches were used to create isogenic human keratinocytes differing only at the identified variant rs11652075, and caspase recruitment domain family member 14 (CARD14)-deficient keratinocytes for subsequent mechanistic studies.
resultsThe genome-wide association study identified the CARD14 rs11652075 variant to be associated with FLG expression in non(never)-lesional skin of children with AD. Rs11652075 is a CARD14 expression quantitative trait locus in human skin and primary human keratinocytes. The T variant destroys a functional cytosine-phosphate-guanine site, resulting in reduced cytosine-phosphate-guanine methylation at this site (but not neighboring sites) in TT and CT compared with CC primary human keratinocytes and Mechanisms of Progression of Atopic Dermatitis to Asthma in Children children's skin samples, and rs11652075 increases CARD14 expression in an allele-specific fashion. Furthermore, studies in clustered regularly interspaced short palindromic repeat-generated CC and TT isogenic keratinocytes, as well as CARD14-haplosufficient and deficient keratinocytes, reveal that IL-17A regulates FLG expression via CARD14, and that the underlying mechanisms are dependent on the rs11652075 genotype.
conclusionsOur study identifies CARD14 as a novel regulator of FLG expression in the skin of children with AD. Furthermore, CARD14 regulates skin FLG homeostasis in an rs11652075-dependent fashion.
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