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角质形成细胞在表皮更新和防御中的作用。

The keratinocyte in epidermal renewal and defence.

作者信息

Suter Maja M, Schulze Katja, Bergman Wilhelmina, Welle Monika, Roosje Petra, Müller Eliane J

机构信息

DermFocus, Institute of Animal Pathology, Vetsuisse Faculty, University of Berne, Berne, Switzerland.

出版信息

Vet Dermatol. 2009 Oct;20(5-6):515-32. doi: 10.1111/j.1365-3164.2009.00819.x.

DOI:10.1111/j.1365-3164.2009.00819.x
PMID:20178490
Abstract

Traditionally, keratinocytes have been considered inert constituents of the multilayered epidermis. Today's understanding has fundamentally changed. The keratinocyte is now recognized as an active player in epidermal renewal with key functions in the skin's immune defence. Under homeostatic conditions, keratinocyte progenitor cells are believed to divide symmetrically or asymmetrically, that is they continue to proliferate or go on to terminally differentiate and build up the overlaying epidermis. The fine-tuned process of epidermal renewal relies on an extraordinary network of signalling cascades which are governed by keratinocyte-receptor interactions with the environment through paracrine and autocrine circuits. Opposing this coordinated homeostatic process are signals of wounding and inflammation. They alter the fate of the keratinocyte and its response to the environment through changes in adhesion molecules and surface receptors, in addition to triggering an immediate inflammatory keratinocyte response in terms of secretion of cytokines, chemokines and antimicrobial peptides. If uncontrolled, the fundamental changes imposed by wounding and inflammation upon the homeostatic programme can lead to severe skin lesions including chronic inflammatory disorders. This review will describe the current knowledge of the regulatory signalling network which allows the keratinocyte to actively impact both epidermal homeostasis and the inflammatory response.

摘要

传统上,角质形成细胞一直被视为多层表皮的惰性成分。如今的认识已发生了根本性的改变。角质形成细胞现在被认为是表皮更新中的活跃参与者,在皮肤免疫防御中具有关键作用。在稳态条件下,角质形成细胞祖细胞被认为会进行对称或不对称分裂,也就是说它们会继续增殖或进入终末分化,从而构建覆盖的表皮。表皮更新的精细过程依赖于一个由信号级联组成的非凡网络,这些信号级联由角质形成细胞通过旁分泌和自分泌回路与环境的受体相互作用所调控。与这种协调的稳态过程相反的是伤口和炎症信号。它们通过改变黏附分子和表面受体来改变角质形成细胞的命运及其对环境的反应,此外还会引发角质形成细胞在细胞因子、趋化因子和抗菌肽分泌方面的即时炎症反应。如果不受控制,伤口和炎症对稳态程序造成的根本性改变可能会导致严重的皮肤病变,包括慢性炎症性疾病。本综述将描述目前关于调节信号网络的知识,该网络使角质形成细胞能够积极影响表皮稳态和炎症反应。

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