The IL-23/IL-17 axis in psoriatic arthritis

被引:127
|
作者
Suzuki, Erika [1 ]
Mellins, Elizabeth D. [2 ,3 ]
Gershwin, M. Eric [1 ]
Nestle, Frank O. [4 ]
Adamopoulos, Iannis E. [1 ,5 ]
机构
[1] Univ Calif Davis, Dept Internal Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA
[2] Stanford Univ, Program Immunol, Div Human Gene Therapy, Palo Alto, CA 94305 USA
[3] Stanford Univ, Program Immunol, Div Pediat Rheumatol, Palo Alto, CA 94305 USA
[4] Kings Coll London, St Johns Inst Dermatol, Div Genet & Mol Med, Sch Med,Guys Hosp, London WC2R 2LS, England
[5] Shriners Hosp Children Northern Calif, Inst Pediat Regenerat Med, Sacramento, CA 95817 USA
关键词
IL-17; IL-23; Psoriatic arthritis; NF-kappa B; NF-KAPPA-B; COLLAGEN-INDUCED ARTHRITIS; T-CELL SUBSET; OSTEOCLAST DIFFERENTIATION; RECEPTOR ACTIVATOR; CUTTING EDGE; NEUTROPHIL RECRUITMENT; RHEUMATOID-ARTHRITIS; JOINT INFLAMMATION; CHEMOKINE RELEASE;
D O I
10.1016/j.autrev.2014.01.050
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 an immune-mediated chronic inflammatory disease, affecting both the skin and joints. Disease progression is associated with aberrant cytokine expression, and TNF blockade is the most successful therapy to date. However, not all patients are responsive to anti-TNF treatment, highlighting the need to better understand the cellular and molecular mechanisms that govern the disease. PsA associations with single nucleotide polymorphisms in IL23R as well as TRAF3IP2 (Act1), a molecule downstream of the IL-17 receptor (IL-17R), have linked the IL-23/IL-17 axis to disease pathology. Although both cytokines are implicated in PsA, a full picture of their cellular targets and pathogenic mechanisms has not yet emerged. In this review, we focus on the IL-23/IL-17 axis-elicited responses mediated by osteoclasts, keratinocytes and neutrophils. Expanding our understanding of the cellular and molecular mechanisms that dictate pathogenicity in PsA will contribute to developing novel treatment strategies to combat disease. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:496 / 502
页数:7
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