Schön Michael P, Erpenbeck Luise
Department of Dermatology, Venereology and Allergology, University Medical Center Göttingen, Göttingen, Germany.
Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen, University of Osnabrück, Osnabrück, Germany.
Front Immunol. 2018 Jun 15;9:1323. doi: 10.3389/fimmu.2018.01323. eCollection 2018.
Research into the pathophysiology of psoriasis has shed light onto many fascinating immunological interactions and underlying genetic constellations. Most prominent among these is the crosstalk between components of the innate and the adaptive immune system and the crucial role of interleukins (IL)-23 and -17 within this network. While it is clear that IL-23 drives and maintains the differentiation of Th17 lymphocytes, many aspects of the regulation of IL-23 and IL-17 are not quite as straightforward and have been unraveled only recently. For example, we know now that Th17 cells are not the only source of IL-17 but that cells of the innate immune system also produce considerable amounts of this central effector cytokine. In addition, there is IL-23-independent production of IL-17. Besides other innate immune cells, neutrophilic granulocytes prominently contribute to IL-17-related immune regulations in psoriasis, and it appears that they employ several mechanisms including the formation of neutrophil extracellular traps. Here, we strive to put the central role of the IL-23/IL-17 axis into perspective within the crosstalk between components of the innate and the adaptive immune system. Our aim is to better understand the complex immune regulation in psoriasis, a disorder that has become a model disease for chronic inflammation.
对银屑病病理生理学的研究揭示了许多迷人的免疫相互作用和潜在的基因组合。其中最突出的是先天性免疫系统和适应性免疫系统各组成部分之间的相互作用，以及白细胞介素（IL）-23和-17在这个网络中的关键作用。虽然很明显IL-23驱动并维持Th17淋巴细胞的分化，但IL-23和IL-17的调节的许多方面并非如此简单直接，直到最近才被揭示出来。例如，我们现在知道Th17细胞不是IL-17的唯一来源，先天性免疫系统的细胞也会产生大量这种核心效应细胞因子。此外，存在不依赖IL-23的IL-17产生。除了其他先天性免疫细胞外，嗜中性粒细胞在银屑病中对IL-17相关的免疫调节有显著贡献，而且它们似乎采用了多种机制，包括形成中性粒细胞胞外陷阱。在这里，我们努力在先天性免疫系统和适应性免疫系统各组成部分之间的相互作用中审视IL-23/IL-17轴的核心作用。我们的目标是更好地理解银屑病中的复杂免疫调节，银屑病已成为慢性炎症的模型疾病。
