Peeling off the genetics of atopic dermatitis–like congenital disorders

Samuelov, Liat; Sprecher, Eli

doi:10.1016/j.jaci.2014.07.061

Cited by 55 publications

(58 citation statements)

References 117 publications

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“…A substantial amount of information, however, indicates that loss of function mutations in serine protease inhibitors (e.g. SPINK5), augments protease activated pathways that enhance Th2 responses supporting the argument that epidermal barrier dysfunction can induce allergic skin diseases (23). This complexity in epidermal gene variants is further modified by variants in genes that control innate and adaptive immune responses (reviewed in references 9 and 51).…”

Section: Complex Causes Of Epithelial Skin Barrier Dysfunction In Admentioning

confidence: 98%

“…Identification of immune pathway polarity will be of particular importance as biologics become more readily available to target specific immune pathways such as Th2 and Th22 pathways as well as various inflammatory cytokines and mediators (20,21). This month's JACI theme focuses particularly on the importance of both genetic and acquired causes of epithelial skin barrier dysfunction in driving the natural history of AD (22)(23)(24). Two original articles this month report that early emollient use to protect the skin barrier may prevent AD (25,26).…”

Section: Introductionmentioning

confidence: 99%

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Deciphering the complexities of atopic dermatitis: Shifting paradigms in treatment approaches

2014

Journal of Allergy and Clinical Immunology

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Atopic dermatitis (AD) is the most common chronic inflammatory skin disease. It often precedes the development of food allergy and asthma. Recent insights into AD reveal abnormalities in terminal differentiation of the epidermal epithelium leading to a defective stratum corneum, which allows enhanced allergen penetration and systemic IgE sensitization. Atopic skin is also predisposed to colonization or infection by pathogenic microbes, most notably Staphylococcus aureus and herpes simplex virus (HSV). Causes of this abnormal skin barrier are complex and driven by a combination of genetic, environmental and immunologic factors. These factors likely account for the heterogeneity of AD onset, severity and natural history of this skin disease. Recent studies suggest prevention of AD can be achieved by early interventions protecting the skin barrier. Onset of lesional AD requires effective control of local and systemic immune activation for optimal management. Early intervention may improve long term outcomes for AD and reduce the systemic allergen sensitization leading to associated allergic diseases in the gastrointestinal and respiratory tract.

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Section: Complex Causes Of Epithelial Skin Barrier Dysfunction In Admentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Deciphering the complexities of atopic dermatitis: Shifting paradigms in treatment approaches

2014

Journal of Allergy and Clinical Immunology

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“…Corneocytes contain abundant keratin: approximately 60% of their dry weight is keratin proteins [12,13]. In epidermal barrier formation, proteins encoded by the keratin (KRT) 1, 2 and 10 genes are implicated with pivotal roles [13].…”

Section: Genetics Of the Epidermal Barrier And Associated Diseasesmentioning

confidence: 99%

“…In epidermal barrier formation, proteins encoded by the keratin (KRT) 1, 2 and 10 genes are implicated with pivotal roles [13]. The cornified envelopes of the corneocytes contain a large amount of filaggrins, which are associated with keratin intermediate filaments and packed into bundles [14,15].…”

Section: Genetics Of the Epidermal Barrier And Associated Diseasesmentioning

confidence: 99%

Pharmacological Targeting of the Epidermal Barrier

Kemény¹,

Nagy²,

Csoma³

et al. 2016

CPD

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The most important function of the skin is to form a barrier between the body and the external environment. The epidermal barrier prevents transepidermal water loss from the skin, but also serves as a barrier to the entry of harmful environmental allergic, toxic or infectious substances. Inherited defects in the genes encoding the components of the epidermal barrier result in the development of rare genetic disorders, whereas polymorphisms in these genes together with environmental factors cause frequent inflammatory skin diseases, such as atopic dermatitis. In this review, components of the skin-barrier function will be reviewed with special emphasis on how the altered epidermal barrier might be repaired. The different strategies to increase the transdermal penetration of drugs is also discussed.3

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“…Тем не менее проникновение в суть генетически обусловленных эпидермальных дефектов, которые способствуют развитию АтД, сместили фокус проблемы в сторону нарушения эпидермального барьера [20]. Важно отметить, что нарушенный эпидермальный барьер не ограничивается дефектами структурных бел-ков кожи и встречается не только у носителей мутации гена белка филаггрина.…”

Section: факторы риска развитияunclassified