Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK.
Immunology. 2020 Aug;160(4):311-312. doi: 10.1111/imm.13237.
Inflammation in psoriasis is driven through the IL-23/IL-17 pathway. Monoclonal antibodies targeting cytokines in the pathway have proven highly effective and are widely used in clinical practice. There is still much to learn, however, about how these pathogenic responses are controlled, particularly with respect to the highly immunologically active molecules produced by the inflamed skin tissue itself. These tissue-derived molecules, which include IL-33, play important roles in modulating chronic inflammation that we are only beginning to understand. Here we highlight new research indicating a role for IL-33 in modulating the inflammatory Th17 response in psoriasis, which may provide avenues for developing new psoriasis treatments.
银屑病中的炎症是通过 IL-23/IL-17 途径驱动的。靶向该途径中细胞因子的单克隆抗体已被证明非常有效,并且广泛应用于临床实践。然而,关于这些致病反应是如何被控制的,我们还有很多需要了解,特别是关于炎症皮肤组织本身产生的高度免疫活性分子。这些组织来源的分子,包括 IL-33,在调节我们才刚刚开始理解的慢性炎症中发挥着重要作用。在这里,我们强调了新的研究表明 IL-33 在调节银屑病中的炎症 Th17 反应中的作用,这可能为开发新的银屑病治疗方法提供途径。