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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >p38MAPK inhibition prevents disease in pemphigus vulgaris mice
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p38MAPK inhibition prevents disease in pemphigus vulgaris mice

机译：p38MAPK抑制可预防寻常性天疱疮小鼠的疾病

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Pemphigus vulgaris (PV) is a life-threatening autoimmune blistering skin disease characterized by detachment of keratinocytes (acantholysis). It has been proposed that PV IgG might trigger signaling and that this process may lead to acantholysis. Indeed, we recently identified a rapid and dose-dependent phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) and heat shock protein (HSP) 27 after binding of PV antibodies to cultured keratinocytes. In human keratinocyte cultures, inhibitors of p38MAPK prevented PV IgG-induced phosphorylation of HSP27 and, more importantly, prevented the early cytoskeletal changes associated with loss of cell-cell adhesion. This study was undertaken to (i) determine whether p38MAPK and HSP25, the murine HSP27 homolog, were similarly phosphorylated in an in vivo model of PV and (h) investigate the potential therapeutic use of p38MAPK inhibition to block blister formation in an animal model of PV. We now report that p38MAPK inhibitors prevented PV blistering disease in vivo. Targeting the end-organ by inhibiting keratinocyte desmosome signaling may be effective for treating desmosome autoimmune blistering disorders.
机译：寻常性天疱疮（PV）是一种威胁生命的自身免疫性水疱性皮肤病，其特征在于角质形成细胞分离（棘皮松解症）。已经提出PV IgG可能触发信号传导，并且该过程可能导致棘层松解术。实际上，我们最近发现，PV抗体与培养的角质形成细胞结合后，p38丝裂原活化蛋白激酶（p38MAPK）和热休克蛋白（HSP）27迅速且呈剂量依赖性磷酸化。在人角质形成细胞培养物中，p38MAPK抑制剂可防止PV IgG诱导的HSP27磷酸化，更重要的是，可防止与细胞-细胞粘附丧失相关的早期细胞骨架变化。进行这项研究的目的是：（i）确定p38MAPK和HSP25（鼠类HSP27同源物）在PV的体内模型中是否被类似地磷酸化，（h）研究p38MAPK抑制作用在动物模型中抑制水泡形成的潜在治疗用途。 PV。现在，我们报道p38MAPK抑制剂在体内预防了PV水疱病。通过抑制角质形成细胞的桥粒体信号传导靶向末端器官可能有效治疗桥粒体自身免疫性水疱性疾病。

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