***，又名银屑病，是一种常见的慢性皮肤病，其特征是出现大小不等的**，红斑，表面覆盖着银白色鳞屑，边界清楚。据调查，银屑病的发病率占据全世界人口的0.1%-3%。由于该病顽固难治，被列为当今世界皮肤科领域的重要研究课题，是全世界皮肤科重点防治**之一。过去的研究表明，***的发生是因为机体的**系统发出了虚假的危险信号，这些信号可激活被称作炎性体的蛋白复合体并提高机体对损伤的炎症反应，导致皮肤上的***块的爆发。近期亦有研究证实自由流动的或细胞质中的DNA与***的炎症有关。
在这篇文章中，JürgenSchauber及其同事从***患者身上进行皮肤活检，并将有病的皮肤细胞与健康志愿者者的皮肤细胞进行比较，证实在***患者的角质化细胞中具有大量的细胞溶质DNA。通过从皮肤样本中萃取RNA并对其基因表达的水平进行检查后，研究人员发现一种编码某个被称作AIM2受体的基因在罹患***病人的皮肤中被高度激活。AIM2 与其它蛋白合作而组装成为炎性体。 该炎性体接着会激活白细胞介素1β，这是驱动炎症的主要物质之一。
在进一步的研究中，Jürgen Schauber等证实一种称之为cathelicidinLL-37的**肽能够与DNA结合，中和角质化细胞中的细胞溶质DNA，阻断AIM2炎性体激活。进而研究人员发现维生素D控制着皮肤中cathelicidin的产生，并能增加cathelicidin与DNA的结合。维生素D通过增进cathelicidin与DNA的结合而帮助防止了DNA对AIM2 受体和触发炎症反应的炎性体的激活。
目前人们常采用外用性维生素D及UVB射线（它可激活维生素D）来*****这一慢性、自身**性皮肤病。新研究发现帮助解释了维生素D疗法为何能够成功地*****及注入皮肤干燥或湿疹等相关性皮肤病，即维生素D对抗***炎症反应的机制，并为这一慢性皮肤**提供了新的有潜力的**靶点。
推荐原文摘要：
Cytosolic DNA Triggers Inflammasome Activation in Keratinocytesin Psoriatic Lesions
The proinflammatory cytokine interleukin-1β (IL-1β) plays acentral role in the pathogenesis and the course of inflammatoryskin diseases, including psoriasis. Posttranscriptional activationof IL-1β is mediated by inflammasomes; however, the mechanismstriggering IL-1β processing remain unknown. Recently, cytosolic DNAhas been identified as a danger signal that activates inflammasomescontaining the DNA sensor AIM2. In this study, we detected abundantcytosolic DNA and increased AIM2 expression in keratinocytes inpsoriatic lesions but not in healthy skin. In culturedkeratinocytes, interferon-γ induced AIM2, and cytosolic DNAtriggered the release of IL-1β via the AIM2 inflammasome. Moreover,the antimicrobial cathelicidin peptide LL-37, which can interactwith DNA in psoriatic skin, neutralized cytosolic DNA inkeratinocytes and blocked AIM2 inflammasome activation. Together,these data suggest that cytosolic DNA is an importantdisease-associated molecular pattern that can trigger AIM2inflammasome and IL-1β activation in psoriasis. Furthermore,cathelicidin LL-37 interfered with DNA-sensing inflammasomes, whichthereby suggests an anti-inflammatory function for this peptide.Thus, our data reveal a link between the AIM2 inflammasome,cathelicidin LL-37, and autoinflammation in psoriasis, providingnew potential targets for the treatment of this chronic skindisease.