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作为变应原暴露途径的皮肤:第二部分。变应原以及微生物群和环境暴露的作用。

The Skin as a Route of Allergen Exposure: Part II. Allergens and Role of the Microbiome and Environmental Exposures.

作者信息

Knaysi George, Smith Anna R, Wilson Jeffrey M, Wisniewski Julia A

机构信息

Department of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA.

Geisel School of Medicine, Dartmouth College, 1 Rope Ferry Road, Hanover, NH, 03755, USA.

出版信息

Curr Allergy Asthma Rep. 2017 Jan;17(1):7. doi: 10.1007/s11882-017-0675-4.

Abstract

PURPOSE OF REVIEW

This second part of the article aims to highlight recent contributions in the literature that enhance our understanding of the cutaneous immune response to allergen.

RECENT FINDINGS

Several properties of allergens facilitate barrier disruption and cutaneous sensitization. There is a strong epidemiologic relationship between the microbiome, both the gut and skin, and atopic dermatitis (AD). The mechanisms connecting these two entities remain enigmatic; however, recent murine models show that commensal skin bacteria play an active role in supporting skin barrier homeostasis and defense against microbial penetration. Likewise, the association between the lack of colonization with Staph species and AD development suggests a potentially functional role for these organisms in regulating the skin barrier and response to environmental allergens. In undisrupted skin, evidence suggests that the cutaneous route may promote allergen tolerance. Properties of environmental allergens and commensal bacteria add to the complex landscape of skin immunity. Further investigation is needed to elucidate how these properties regulate the cutaneous immune response to allergen.

摘要

综述目的

本文的第二部分旨在强调文献中最近的研究成果,这些成果增进了我们对皮肤对过敏原免疫反应的理解。

最新发现

过敏原的若干特性有助于破坏屏障并引发皮肤致敏。肠道和皮肤微生物群与特应性皮炎(AD)之间存在密切的流行病学关系。连接这两个实体的机制仍然不明;然而,最近的小鼠模型表明,皮肤共生细菌在支持皮肤屏障稳态和抵御微生物侵入方面发挥着积极作用。同样,缺乏葡萄球菌属细菌定植与AD发展之间的关联表明这些微生物在调节皮肤屏障和对环境过敏原的反应中可能具有功能性作用。在未受破坏的皮肤中,有证据表明经皮途径可能促进过敏原耐受性。环境过敏原和共生细菌的特性增加了皮肤免疫的复杂情况。需要进一步研究以阐明这些特性如何调节皮肤对过敏原的免疫反应。

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