Insights into atopic dermatitis gained from genetically defined mouse models

• Published in: Journal of allergy and clinical immunology Vol. 143; no. 1; pp. 13 - 25
• Main Authors: Nakajima, Saeko, Nomura, Takashi, Common, John, Kabashima, Kenji
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.01.2019; Elsevier Limited
• Subjects: Animal models; Antigens; Atopic dermatitis; Chemokines; Cytokines; Dermatitis; Disease; Eczema; Etiology; genetically defined mouse models; Genotype & phenotype; Helper cells; Human subjects; immune dysfunction; Immune response; Immune system; Keratin; Kinases; Lymphocytes; Lymphocytes T; microbiome; Microbiomes; Microbiota; Mutation; Pathogenesis; Proteins; pruritis; Pruritus; Rodents; skin barrier; Skin diseases; TH2 cell response; FLG; skin barrier; immune dysfunction; AD; TRPA1; TSLP; TH2 cell response; KLK; PSM; microbiome; ILC2; STAT; PPAR; Atopic dermatitis; LC; genetically defined mouse models; TLR; pruritis; T(H)2 cell response
• ISSN: 0091-6749; 1097-6825; 1097-6825
• DOI: 10.1016/j.jaci.2018.11.014

Atopic dermatitis (AD) is characterized by severe pruritus and recurrent eczema with a chronic disease course. Impaired skin barrier function, hyperactivated TH2 cell–type inflammation, and pruritus-induced scratching contribute to the disease pathogenesis of AD. Skin microbial alterations complicate the pathogenesis of AD further. Mouse models are a powerful tool to analyze such intricate pathophysiology of AD, with a caution that anatomy and immunology of the skin differ between human subjects and mice. Here we review recent understanding of AD etiology obtained using mouse models, which address the epidermal barrier, skin microbiome, TH2 immune response, and pruritus.