皮肤作为变应原暴露途径：第一部分。免疫成分与机制。
The Skin as a Route of Allergen Exposure: Part I. Immune Components and Mechanisms.
作者信息
Smith Anna R, Knaysi George, Wilson Jeffrey M, Wisniewski Julia A
机构信息
Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA.
Department of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA.
出版信息
Curr Allergy Asthma Rep. 2017 Jan;17(1):6. doi: 10.1007/s11882-017-0674-5.
Abstract
PURPOSE OF REVIEW
To highlight recent contributions in the literature that enhance our understanding of the cutaneous immune response to allergen.
RECENT FINDINGS
Defects in skin barrier function in infancy set the stage for the development of atopic dermatitis (AD) and allergy. Both genetic and environmental factors can contribute to damage of the stratum corneum (SC), with activation of specific protease enzymes under high pH conditions playing a key role. Immune cells and mediators in the dermis and epidermis impair SC repair mechanisms and support allergy development. In barrier-disrupted skin, type 2 innate lymphoid cells (ILC2s), mast cells (MCs), and basophils have been shown to promote AD and pathogenic Th2 responses in murine models. Skin barrier disruption favors induction of systemic Th2-associated inflammatory pathways. A better understanding of the ontogeny and regulation of these complex networks in infant skin is needed to guide future strategies for allergy treatment and prevention.
摘要
综述目的
强调文献中近期的研究成果，这些成果增进了我们对皮肤对变应原免疫反应的理解。
最新发现
婴儿期皮肤屏障功能缺陷为特应性皮炎（AD）和过敏的发展奠定了基础。遗传和环境因素均可导致角质层（SC）受损，高pH条件下特定蛋白酶的激活起关键作用。真皮和表皮中的免疫细胞及介质会损害SC修复机制并促进过敏发展。在屏障受损的皮肤中，2型固有淋巴细胞（ILC2s）、肥大细胞（MCs）和嗜碱性粒细胞在小鼠模型中已被证明可促进AD和致病性Th2反应。皮肤屏障破坏有利于诱导全身性Th2相关炎症途径。需要更好地理解婴儿皮肤中这些复杂网络的个体发生和调控，以指导未来过敏治疗和预防策略。
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