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首页> 外文期刊>The Journal of investigative dermatology. >Vitamin D analog calcipotriol suppresses the Th17 cytokine-induced proinflammatory S100 alarmins psoriasin (S100A7) and koebnerisin (S100A15) in psoriasis
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Vitamin D analog calcipotriol suppresses the Th17 cytokine-induced proinflammatory S100 alarmins psoriasin (S100A7) and koebnerisin (S100A15) in psoriasis

机译：维生素D类似物卡泊三醇抑制牛皮癣中Th17细胞因子诱导的促炎性S100警报蛋白psoriasin（S100A7）和koebnerisin（S100A15）

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The antimicrobial peptides (AMP) psoriasin (S100A7) and koebnerisin (S100A15) are differently induced in psoriatic skin. They act synergistically as chemoattractants and alarmins to amplify inflammation in psoriasis. Th17 cytokines are key players in psoriasis pathogenesis and vitamin D analogs feature anti-psoriatic effects; both of these activities could be mediated through epidermal AMP regulation. We show that supernatants of cultured psoriatic T cells induce and release psoriasin and koebnerisin from keratinocytes and the Th17 cytokines IL-17A, tumor necrosis factor-α, and IL-22 differently regulate psoriasin and koebnerisin reflecting their distinct expression pattern in normal and psoriatic skin. IL-17A is the principal inducer of both S100 and their expression is further amplified by cooperating Th17 cytokines in the micromilieu of psoriatic skin. Increased extracellular psoriasin and koebnerisin also synergize as alarmins to prime epidermal keratinocytes for production of immunotropic cytokines that further amplify the inflammatory response. Treatment of psoriatic plaques with the vitamin D analog calcipotriol interferes with the S100-mediated positive feedback loop by suppressing the increased production of psoriasin and koebnerisin in psoriatic skin and their Th17-mediated regulation in epidermal keratinocytes. Thus, targeting the S100-amplification loop could be a beneficial anti-inflammatory approach in psoriasis and other inflammatory skin diseases.
机译：银屑病皮肤中诱导抗菌肽（AMP）的牛皮癣素（S100A7）和科布尼菌素（S100A15）的方式有所不同。它们协同作用作为趋化剂和警报蛋白，以扩大牛皮癣中的炎症。 Th17细胞因子是牛皮癣发病的关键因素，维生素D类似物具有抗银屑病的作用;这两种活动都可以通过表皮AMP调节介导。我们显示培养的牛皮癣T细胞的上清液诱导并从角质形成细胞中释放牛皮癣素和koebnerisin，Th17细胞因子IL-17A，肿瘤坏死因子-α和IL-22不同地调节牛皮癣和koebnerisin，反映了它们在正常和牛皮癣皮肤中的独特表达模式。 IL-17A既是S100的主要诱导剂，又可以通过在银屑病皮肤微环境中协同Th17细胞因子来进一步扩增它们的表达。增加的胞外psoriasin和koebnerisin还可以作为警报蛋白协同作用于表皮角质形成细胞，以产生可进一步放大炎症反应的免疫细胞因子。用维生素D类似物卡泊三醇治疗牛皮癣斑块，通过抑制牛皮癣皮肤中牛皮癣菌素和koebnerisin的生产增加以及表皮角质形成细胞中Th17介导的调节，干扰了S100介导的正反馈回路。因此，在牛皮癣和其他炎症性皮肤病中，靶向S100扩增环可能是一种有益的抗炎方法。

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