T helper type 2 signatures in atopic dermatitis. Issue 3 (25th July 2018)

• Record Type: Journal Article
• Authors: Furue, Masutaka
• Is Part Of: Journal of cutaneous immunology and allergy. Volume 1:Issue 3(2018)
• Page Start: 93
• Page End: 99
• Publication Date: 2018-07-25
• Subjects: atopic dermatitis -- CCL17 -- dupilumab -- filaggrin -- IgE -- T helper type 2; Skin -- Diseases -- Immunological aspects -- Periodicals; Skin -- Diseases -- Periodicals; Skin -- Diseases -- Treatment -- Periodicals; 616.5079
• DOI: 10.1002/cia2.12023
• Languages: English
• ISSNs: 2574-4593

Abstract

Abstract: T helper type 2 (Th2)‐derived cytokines, such as IL‐4, IL‐13, and IL‐31, play a fundamental role in the development and progression of atopic dermatitis (AD). In addition to gene mutations of filaggrin (FLG), the Th2‐deviated microenvironment downregulates FLG expression and disrupts barrier function, resulting in Staphylococcus aureus colonization and increased penetration of external allergens. From lesional AD skin, the Th2 milieu helps to release Th2‐related chemokines such as CCL17, CCL22, and CCL26, which augment recruitment of Th2 cells and eosinophils. IL‐4 and IL‐13 stimulate B cells to produce IgE that links AD to other atopic comorbidities. IL‐31 is the major pruritogenic cytokine in AD. Notably, the anti–IL‐4 receptor α antibody dupilumab and the anti–IL‐31 receptor A antibody nemolizumab have proven to be effective for treatment of AD. In the present review, Th2 signatures in AD are examined and overviewed. Abstract : T helper type 2 signatures in atopic dermatitis are highlighted.