作者: Robert Gruber , Christian Börnchen , Katharina Rose , Anne Daubmann , Thomas Volksdorf
DOI: 10.1016/J.AJPATH.2015.06.021
关键词: Pathogenesis 、 Occludin 、 Biology 、 Keratinocyte 、 Barrier function 、 Immunology 、 Tight junction 、 Claudin 、 Atopic dermatitis 、 Interleukin 13
摘要: Tight junctions are important for skin barrier function. The tight junction protein claudin 1 (Cldn-1) has been reported to be down-regulated in nonlesional of atopic dermatitis (AD) patients. In contrast, we did not observe a significant down-regulation Cldn-1 the AD cohort used this study. However, first time, upper and lower epidermal layers lesional was detected. addition, there up-regulation Cldn-4 nonlesional, but lesional, skin. For occludin, no alterations were observed. an AD-like allergic mouse model, eczema significantly influenced by dermal inflammation, correlated with hallmarks (ie, increased keratinocyte proliferation, altered differentiation, thickness, impaired function). human equivalents, addition IL-4, IL-13, IL-31 resulted Cldn-1, Cldn1 knockdown keratinocytes abnormal differentiation. summary, provide evidence that differentially involved pathogenesis. Our data suggest role formation triggered inflammation.