Pathophysiology and inhibition of IL-23 signaling in psoriatic arthritis: A molecular insight

被引：24
作者：
Cuong Thach Nguyen [1 ]
Bloch, Yehudi [2 ,3 ]
Skladanowska, Katarzyna [2 ,3 ]
Savvides, Savvas N. [2 ,3 ]
Adamopoulos, Iannis E. [1 ,4 ]
机构：
[1] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Dept Internal Med, Davis, CA 95616 USA
[2] Univ Ghent, Dept Biochem & Microbiol, Technol Pk 927, B-9052 Ghent, Belgium
[3] VIB Ctr Inflammat Res, Technol Pk 927, B-9052 Ghent, Belgium
[4] Shriners Hosp Children Northern Calif, Inst Pediat Regenerat Med, Sacramento, CA 95817 USA
来源：
CLINICAL IMMUNOLOGY | 2019年 / 206卷
基金：
美国国家卫生研究院;
关键词：
Psoriatic arthritis; Skin and joint inflammation; Cytokines; IL-23/IL-23R pathways; Human monoclonal IL-23 antibodies; Therapeutics; EXTRACELLULAR TRAP FORMATION; T-CELL SUBSET; DOUBLE-BLIND; MONOCLONAL-ANTIBODY; EPIDERMAL HYPERPLASIA; TERMINAL DIFFERENTIATION; RHEUMATOID-ARTHRITIS; OSTEOCLAST FORMATION; CYTOKINE RECEPTOR; PLACEBO;
D O I：
10.1016/j.clim.2018.09.002
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
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.
引用
收藏
页码：15 / 22
页数：8
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