Epithelial immune crosstalk with the skin microbiota in homeostasis and atopic dermatitis - a mini review -
Epithelial immune crosstalk with the skin microbiota in homeostasis and atopic dermatitis - a mini review -
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上皮免疫与皮肤微生物群在稳态和特应性皮炎中的相互作用 - 一个简短的评论 -
DOI：
10.1111/vde.13007
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发表时间：
2021
影响因子：
1.4
通讯作者：
Imanishi Ichiro
中科院分区：
文献类型：
--
作者：
Kobayashi Tetsuro;Imanishi Ichiro
皮肤是一个复杂而动态的生态系统，其中上皮细胞、免疫细胞和皮肤微生物群积极相互作用并维持屏障完整性和功能性免疫。皮肤微生物主动调节常驻免疫细胞的功能。菌群失调--常驻微生物群的改变--导致宿主免疫功能失调。对患有特应性皮炎（AD）的人和狗进行的微生物组分析显示，微生物多样性发生了变化，特别是葡萄球菌的比例增加。表现出AD样症状的单基因疾病从上皮和免疫学角度提供了对AD发病机制和生态失调机制的见解。宿主和微生物群之间的共生关系必须组成性地维持。宿主免疫如何调节稳态下的肠道细菌的详细机制已被报道。皮肤含有多种组织驻留免疫细胞，包括先天性和适应性免疫细胞。最近的研究强调了先天性淋巴样细胞（ILC）在维持屏障功能和组织稳态中的基本作用。ILC直接响应组织来源的信号，并有助于屏障免疫。上皮细胞产生alarmins，如胸腺基质淋巴细胞生成素（TSLP）和白细胞介素（IL）-33和IL-25，所有这些都激活2型ILC（ILC 2），产生2型细胞因子，如IL-5和IL-13，增强2型免疫反应。上皮-ILC串扰的失调导致过敏性炎症。这篇综述强调了我们对宿主上皮细胞和免疫细胞以及微生物群之间的积极相互作用的理解，为炎症性皮肤病的新治疗策略提供了基础。
The skin is a complex and dynamic ecosystem, wherein epithelial cells, immune cells and the skin microbiota actively interact and maintain barrier integrity and functional immunity. Skin microbes actively tune the functions of the resident immune cells. Dysbiosis – alterations in the resident microbiota – leads to the dysregulation of host immunity. Microbiome analyses in humans and dogs with atopic dermatitis (AD) have shown shifts in microbial diversity, and in particular, an increased proportion of staphylococci. Monogenic diseases that manifest AD‐like symptoms provide insights into the pathogenesis of AD and the mechanisms of dysbiosis, from both the epithelial and immunological perspectives. The symbiotic relationships between the host and microbiota must be maintained constitutively. Detailed mechanisms of how host immunity regulates commensal bacteria in the steady state have been reported. The skin harbours multiple tissue‐resident immune cells, including both innate and adaptive immune cells. Recent studies have highlighted the fundamental role of innate lymphoid cells (ILCs) in the maintenance of barrier functions and tissue homeostasis. ILCs directly respond to tissue‐derived signals and are instrumental in barrier immunity. Epithelial cells produce alarmins such as thymic stromal lymphopoietin (TSLP) and interleukins (IL)‐33 and IL‐25, all of which activate group 2 ILCs (ILC2s), which produce type 2 cytokines, such as IL‐5 and IL‐13, boosting type 2 immune reactions. Dysregulation of the epithelial–ILC crosstalk results in allergic inflammation. This review highlights our understanding of the active interactions between the host epithelial and immune cells, and microbiota, providing a foundation for novel therapeutic strategies for inflammatory skin diseases.