| Literature DB >> 30612664 |
Saeko Nakajima1, Takashi Nomura1, John Common2, Kenji Kabashima3.
Abstract
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.Entities:
Keywords: Atopic dermatitis; T(H)2 cell response; genetically defined mouse models; immune dysfunction; microbiome; pruritis; skin barrier
Mesh:
Year: 2019 PMID: 30612664 DOI: 10.1016/j.jaci.2018.11.014
Source DB: PubMed Journal: J Allergy Clin Immunol ISSN: 0091-6749 Impact factor: 10.793