Reprint

Therapy and Prevention of Atopic Dermatitis and Psoriasis

Edited by
July 2020
274 pages
  • ISBN978-3-03936-537-1 (Hardback)
  • ISBN978-3-03936-538-8 (PDF)

This is a Reprint of the Special Issue Therapy and Prevention of Atopic Dermatitis and Psoriasis that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

Atopic dermatitis and psoriasis are common inflammatory skin diseases. The excellent therapeutic success of anti-IL-4/IL-13 biologics for atopic dermatitis and anti-TNF-α/IL-23/IL-17A biologics for psoriasis highlights the major pathogenic roles of these cytokines in the respective diseases. Although atopic dermatitis and psoriasis are distinct clinical entities, they share similar inflammatory processes, including increased Th17, Th22, and Th1 signatures. In addition to skin inflammation, both skin diseases exhibit a significant association with systemic diseases such as cardiovascular diseases, metabolic syndrome, and autoimmune diseases. In contrast to atopic dermatitis, males are more susceptible to psoriasis than females. Differential risk factors may be involved in the development and exacerbation in atopic dermatitis and psoriasis. In this issue, we will publish cutting-edge information regarding skin inflammation, clinical aspects, risk factors, microbiome, and therapeutics related to psoriatic and atopic inflammation.

Format
  • Hardback
License and Copyright
© 2020 by the authors; CC BY-NC-ND license
Keywords
scratch injury; IL-13Rα2; keratinocyte; IL-13; atopic dermatitis; IL-4Rα; IL-13Rα1; involucrin; IL-31; IL-31 receptor alpha; Ccl 17; Ccl 22; dendritic cell; atopic dermatitis; lipid mediators; psoriasis vulgaris; psoriatic arthritis; lipid peroxidation products; endocannabinoids; eicosanoids; psoriasis; risk factor; extrinsic risk factor; intrinsic risk factor; onset; exacerbation; butyric acid; microbiome; probiotic; S. epidermidis; UVB; atopic dermatitis; estrogen; progesterone; androgen; dehydroepiandrosterone; T helper 2 cell; skin barrier; aryl hydrocarbon receptor (AHR); aryl hydrocarbon receptor-nuclear translocator (ARNT); nuclear factor-erythroid 2-related factor-2 (NRF2); atopic dermatitis; psoriasis; tapinarof; filaggrin; skin barrier; Th17; Th22; Treg; reactive oxygen species; antioxidants; psoriasis; psoriatic arthritis; osteoimmunological markers; bone resorption; CCL20; IL-17A; psoriasis; scratch injury; epidermal growth factor receptor; Koebner phenomenon; ERK; JNK; p38 MAPK; keratinocyte; psoriasis; tissue resident memory cells; IL-17; lipid; psoriasis; inflammation; atopic dermatitis; serine proteases; kallikrein-related peptidases; epidermal barrier dysfunction; lympho-epithelial Kazal-type-related inhibitor (LEKTI); SPINK5; filaggrin; psoriasis; keratinocytes; interleukin-17A; Th17; ILC3; CCL20; CXCL1; CXCL8; Koebner phenomenon; antimicrobial peptides; IL-22; IL-26; subtypes of atopic dermatitis; ustekinumab; wound healing; antimicrobial peptides; biologics; psoriasis; psoriatic arthritis; tumor necrosis factor-α; inteleukin-23; interluekin-17; psoriasis; tissue resident cells; innate lymphoid cells; regulatory T cells; Foxp3; gut microbiome; systemic inflammation; atopic dermatitis; complicating factors; aggravating factors; triggering factors; irritants; aeroallergens; food; microbial organisms; contact allergens; sweat; scratching; skin inflammation; cytokine; adipose tissue; adiponectin; leptin; thermogenesis