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      Skin Barrier Disruption - A Requirement for Allergen Sensitization?

      , M.D. 1 , , M.D. Ph.D 2 , 3 , , M.D. 1

      The Journal of Investigative Dermatology

      Atopic dermatitis, barrier, epicutaneous sensitization, allergen

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          Abstract

          For at least half a century, noninvasive techniques have been available to quantify skin barrier function, and these have shown that a number of human skin conditions and disorders are associated with defects in skin permeability. In the last decade, several genes responsible for skin barrier defects observed in both monogenetic and complex, polygenic disorders have been elucidated and functionally characterized. This has led to an explosion of work in the last six years that has identified pathways connecting epidermal barrier disruption and antigen uptake as well as the quality and/or magnitude of the antigen-specific adaptive immune response. This review will introduce the notion that diseases arise from the dynamic crosstalk that occurs between the skin barrier and immune system using atopic dermatitis or eczema as the disease prototype. Nevertheless, the concepts put forth are highly relevant to a number of antigen-driven disorders for which skin barrier is at least transiently compromised such as psoriasis, allergic contact dermatitis and blistering disorders.

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          Most cited references 146

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          Development, cytokine profile and function of human interleukin 17-producing helper T cells.

          T(H)-17 cells are a distinct lineage of proinflammatory T helper cells that are essential for autoimmune disease. In mice, commitment to the T(H)-17 lineage is dependent on transforming growth factor-beta and interleukin 6 (IL-6). Here we demonstrate that IL-23 and IL-1beta induced the development of human T(H)-17 cells expressing IL-17A, IL-17F, IL-22, IL-26, interferon-gamma, the chemokine CCL20 and transcription factor RORgammat. In situ, T(H)-17 cells were identified by expression of the IL-23 receptor and the memory T cell marker CD45RO. Psoriatic skin lesions contained IL-23-producing dendritic cells and were enriched in the cytokines produced by human T(H)-17 cells that promote the production of antimicrobial peptides in human keratinocytes. Our data collectively indicate that human and mouse T(H)-17 cells require distinct factors during differentiation and that human T(H)-17 cells may regulate innate immunity in epithelial cells.
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            The cornified envelope: a model of cell death in the skin.

            The epidermis functions as a barrier against the environment by means of several layers of terminally differentiated, dead keratinocytes - the cornified layer, which forms the endpoint of epidermal differentiation and death. The cornified envelope replaces the plasma membrane of differentiating keratinocytes and consists of keratins that are enclosed within an insoluble amalgam of proteins, which are crosslinked by transglutaminases and surrounded by a lipid envelope. New insights into the molecular mechanisms and the physiological endpoints of cornification are increasing our understanding of the pathological defects of this unique form of programmed cell death, which is associated with barrier malfunctions and ichthyosis.
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              IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo.

              We have characterized a cytokine produced by Th2 cells, designated as IL-25. Infusion of mice with IL-25 induced IL-4, IL-5, and IL-13 gene expression. The induction of these cytokines resulted in Th2-like responses marked by increased serum IgE, IgG(1), and IgA levels, blood eosinophilia, and pathological changes in the lungs and digestive tract that included eosinophilic infiltrates, increased mucus production, and epithelial cell hyperplasia/hypertrophy. In addition, our studies show that IL-25 induces Th2-type cytokine production by accessory cells that are MHC class II(high), CD11c(dull), and lineage(-). These results suggest that IL-25, derived from Th2 T cells, is capable of amplifying allergic type inflammatory responses by its actions on other cell types.
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                Author and article information

                Journal
                0426720
                4839
                J Invest Dermatol
                The Journal of Investigative Dermatology
                0022-202X
                1523-1747
                7 December 2011
                5 January 2012
                March 2012
                1 September 2012
                : 132
                : 3
                : 949-963
                Affiliations
                [1 ]Department of Dermatology, University of Rochester Medical Center, Rochester, NY
                [2 ]Department of Dermatology, School of Medicine, Keio University, Tokyo, Japan
                [3 ]Center for Integrated Medical Research, School of Medicine, Keio University, Tokyo, Japan
                Author notes
                Corresponding Author: Lisa A. Beck, M.D., University of Rochester, Dept of Dermatology, 601 Elmwood Ave, Box 697, Rochester, NY 14642, Phone: 585-275-1039, Fax: 585-276-2330, Lisa_Beck@ 123456URMC.ROCHESTER.EDU
                Article
                nihpa340407
                10.1038/jid.2011.435
                3279586
                22217737
                Categories
                Article

                Dermatology

                epicutaneous sensitization, barrier, atopic dermatitis, allergen

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