关键词: JAK/STAT signaling pathway SOCS proteins atopic dermatitis inflammation psoriasis skin

Mesh : Humans Suppressor of Cytokine Signaling Proteins / genetics metabolism Signal Transduction / genetics Cytokines / metabolism Inflammation Dermatitis, Atopic Psoriasis

来  源:   DOI:10.3390/cells13060505   PDF(Pubmed)

Abstract:
Inflammatory skin diseases include a series of disorders characterized by a strong activation of the innate and adaptive immune system in which proinflammatory cytokines play a fundamental role in supporting inflammation. Skin inflammation is a complex process influenced by various factors, including genetic and environmental factors, characterized by the dysfunction of both immune and non-immune cells. Psoriasis (PS) and atopic dermatitis (AD) are the most common chronic inflammatory conditions of the skin whose pathogeneses are very complex and multifactorial. Both diseases are characterized by an immunological dysfunction involving a predominance of Th1 and Th17 cells in PS and of Th2 cells in AD. Suppressor of cytokine signaling (SOCS) proteins are intracellular proteins that control inflammatory responses by regulating various signaling pathways activated by proinflammatory cytokines. SOCS signaling is involved in the regulation and progression of inflammatory responses in skin-resident and non-resident immune cells, and recent data suggest that these negative modulators are dysregulated in inflammatory skin diseases such as PS and AD. This review focuses on the current understanding about the role of SOCS proteins in modulating the activity of inflammatory mediators implicated in the pathogenesis of inflammatory skin diseases such as PS and AD.
摘要:
炎性皮肤病包括一系列病症,其特征在于先天和适应性免疫系统的强烈激活,其中促炎细胞因子在支持炎症中起基本作用。皮肤炎症是一个受多种因素影响的复杂过程,包括遗传和环境因素,以免疫和非免疫细胞功能障碍为特征。银屑病(PS)和特应性皮炎(AD)是最常见的慢性皮肤炎症,其发病机制非常复杂且多因素。两种疾病的特征都是免疫功能障碍,涉及PS中Th1和Th17细胞以及AD中Th2细胞的优势。细胞因子信号传导抑制剂(SOCS)蛋白是通过调节由促炎细胞因子激活的各种信号传导途径来控制炎症反应的细胞内蛋白。SOCS信号参与皮肤驻留和非驻留免疫细胞炎症反应的调节和进展,和最近的数据表明,这些负调节剂在炎症性皮肤病如PS和AD中失调。本文综述了目前对SOCS蛋白在调节与PS和AD等炎症性皮肤病发病机制相关的炎症介质活性中的作用的认识。
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