TLR2 expression is increased in rosacea and stimulates enhanced serine protease production by keratinocytes.
TLR2 expression is increased in rosacea and stimulates enhanced serine protease production by keratinocytes.
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DOI：
10.1038/jid.2010.351
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发表时间：
2011-03
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--
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多样化的环境挑战皮肤，在保持温度、水分和电解质平衡的同时，也保持正常的免疫功能。酒渣鼻是一种常见的皮肤病，对正常环境刺激表现出独特的炎症反应。我们假设天然免疫模式识别功能的异常可以解释酒渣鼻患者对酒渣鼻敏感性增强的原因，并观察到酒渣鼻患者的表皮表达Toll样受体2(TLR2)的量高于正常患者。在特应性皮炎或牛皮癣等其他炎症性皮肤病中未见TLR2表达增加。在角质形成细胞上过表达TLR2，用TLR2配体治疗，以及对TLR2缺乏的小鼠的分析，导致角质形成细胞释放激肽释放酶5，这是一种参与酒渣鼻发病机制的关键蛋白酶。这些观察表明，TLR2功能异常可能解释了对环境刺激的炎症反应增强，并可能在酒渣鼻的发病机制中发挥关键作用。
A diverse environment challenges skin to maintain temperature, hydration, and electrolyte balance while also maintaining normal immunological function. Rosacea is a common skin disease that manifests unique inflammatory responses to normal environmental stimuli. We hypothesized that abnormal function of innate immune pattern recognition could explain the enhanced sensitivity of patients with rosacea, and observed that the epidermis of patients with rosacea expressed higher amounts of Toll-like receptor 2 (TLR2) than normal patients. Increased expression of TLR2 was not seen in other inflammatory skin disorders such as atopic dermatitis or psoriasis. Overexpression of TLR2 on keratinocytes, treatment with TLR2 ligands, and analysis of TLR2-deficient mice resulted in a calcium-dependent release of kallikrein 5 from keratinocytes, a critical protease involved in the pathogenesis of rosacea. These observations show that abnormal TLR2 function may explain enhanced inflammatory responses to environmental stimuli and can act as a critical element in the pathogenesis of rosacea.
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