Department of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, CA, USA.
Department of Biochemistry and Microbiology, Ghent University, Technologiepark 927, Ghent 9052, Belgium; VIB Center for Inflammation Research, Technologiepark 927, Ghent 9052, Belgium.
Clin Immunol. 2019 Sep;206:15-22. doi: 10.1016/j.clim.2018.09.002. Epub 2018 Sep 6.
Psoriatic arthritis (PsA) is a chronic inflammatory arthritis of unknown etiology, and currently the cellular and molecular interactions that dictate its pathogenesis remain elusive. A role of the interleukin-23 (IL-23)/IL-23R (IL-23 receptor) interaction in the development of psoriasis and PsA is well established. As IL-23 regulates the differentiation and activation of innate and adaptive immunity, it pertains to a very complex pathophysiology involving a plethora of effectors and transducers. In this review, we will discuss recent advances on the cellular and molecular pathophysiological mechanisms that regulate the initiation and progression of PsA as well as new therapeutic approaches for IL-23/IL-23R targeted therapeutics.
银屑病关节炎（PsA）是一种病因不明的慢性炎症性关节炎，目前尚不清楚决定其发病机制的细胞和分子相互作用。白细胞介素 23（IL-23）/IL-23 受体（IL-23R）相互作用在银屑病和 PsA 的发展中的作用已得到充分证实。由于 IL-23 调节先天和适应性免疫的分化和激活，因此它与涉及众多效应物和转导物的非常复杂的病理生理学有关。在这篇综述中，我们将讨论调节 PsA 起始和进展的细胞和分子病理生理机制的最新进展，以及针对 IL-23/IL-23R 的新型治疗方法。
