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.

中文翻译：

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银屑病关节炎的病理生理学和IL-23信号的抑制：分子的见解。

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，决定其发病机理的细胞和分子相互作用仍然难以捉摸。白细胞介素23（IL-23）/ IL-23R（IL-23受体）相互作用在银屑病和PsA发生中的作用已得到很好的确立。由于IL-23调节先天性和适应性免疫的分化和激活，因此它涉及非常复杂的病理生理，涉及大量的效应子和传感器。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靶向治疗剂的新治疗方法。