2021
DOI: 10.1016/j.jaci.2020.06.012
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Atopic dermatitis displays stable and dynamic skin transcriptome signatures

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Cited by 88 publications
(94 citation statements)
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References 52 publications
(56 reference statements)
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“…Many patients affected by AD show a personal or a familiar history of atopic diseases, such as asthma, allergic rhinitis, and a specific IgE-reactivity [70]. AD is a multifactorial disease based on a genetic predisposition with the contribution of environmental factors, leading to skin barrier impairment and cutaneous inflammation, which is driven by excessive T cell activation and an increased production of inflammatory cytokines [71]. Genetic susceptibility encompasses the keratinocyte differentiation process, such as filaggrin, with a consequent skin barrier weakness, as well as immune dysregulation with a Th2 immune response.…”
Section: Atopic Dermatitismentioning
confidence: 99%
See 1 more Smart Citation
“…Many patients affected by AD show a personal or a familiar history of atopic diseases, such as asthma, allergic rhinitis, and a specific IgE-reactivity [70]. AD is a multifactorial disease based on a genetic predisposition with the contribution of environmental factors, leading to skin barrier impairment and cutaneous inflammation, which is driven by excessive T cell activation and an increased production of inflammatory cytokines [71]. Genetic susceptibility encompasses the keratinocyte differentiation process, such as filaggrin, with a consequent skin barrier weakness, as well as immune dysregulation with a Th2 immune response.…”
Section: Atopic Dermatitismentioning
confidence: 99%
“…Excessive epidermal colonization by S. aureus is involved in pathogenesis, by damaging the skin barrier and inducing inflammatory responses and immune activation. Type 2 inflammation in AD is characterized by the activation of Th2 cells, T-cytotoxic 2 cells, innate lymphoid cells 2, eosinophils and mast cells, while other immune pathways such as Th22, Th17, Th9, and Th1 might contribute to maintain the pathogenic mechanism [71]. Multiple type 2 cytokines, including IL-4, IL-5, IL-9, IL-13, IL-25, IL-31, IL-33, and TSLP are overexpressed in skin and in the peripheral blood [72].…”
Section: Atopic Dermatitismentioning
confidence: 99%
“…Simultaneous blocking of Type I receptor (IL‐4Rα/γc) and Type 2 receptor (IL‐4Rα/IL‐13Rα) inhibit at the same time T2 responses dependent on IL‐4 and IL‐4/IL‐13, respectively, in hematopoietic and non‐hematopoietic cells. Dupilumab targets several important disease mechanisms in the skin of AD patients, including the skin‐barrier defect, the chronic itch, the microbiome, and the T2 inflammation, both in clinical trials and in real life 38,39,63‐67 . Accumulating experience with dupilumab treatment for AD confirmed its effectiveness and safety, by reducing AD severity, reliever and background medication, and improving QoL, both in the paediatric population 12–17 years old and in adults 68‐77 …”
Section: Key Recommendationsmentioning
confidence: 97%
“…Dupilumab targets several important disease mechanisms in the skin of AD patients, including the skin-barrier defect, the chronic itch, the microbiome, and the T2 inflammation, both in clinical trials and in real life. 38,39,[63][64][65][66][67] Accumulating experience with dupilumab treatment for AD confirmed its effectiveness and safety, by reducing AD severity, reliever and background medication, and improving QoL, both in the paediatric population 12-17 years old and in adults. [68][69][70][71][72][73][74][75][76][77] Recent evidence was published for the efficacy and safety in the 6-11 years old population.…”
Section: Ke Y Recommendationsmentioning
confidence: 99%
“…Crucially, the cytokines IL-4, IL-13 and IL-31 require JAK-STAT downstream signaling for their biological function [ 37 , 38 , 39 ] ( Figure 2 ). Furthermore, AD skin transcriptome analysis revealed increased JAK1 expression in lesional and non-lesional tissue [ 40 ]. In addition to inflammation, pruritic cytokines, thymic stromal lymphopoietin (TSLP) and IL-31 use downstream JAK1 and JAK2 signaling [ 39 , 41 ] ( Figure 3 ).…”
Section: Inflammatory Skin Diseasesmentioning
confidence: 99%