IL-23 Inhibition in Ankylosing Spondylitis: Where Did It Go Wrong?

被引:24
作者
Baeten, Dominique [1 ,2 ]
Adamopoulos, Iannis E. [3 ]
机构
[1] Amsterdam Univ Med Ctr, Clin Immunol & Rheumatol, Amsterdam, Netherlands
[2] UCB, Immunol Therapeut Area, Slough, Berks, England
[3] Beth Israel Med Deaconess Ctr, Dept Med, Div Rheumatol & Clin Immunol, Boston, MA USA
关键词
interleukin-23; interleukin-17; ankylosing spondylitis; axial spondyloarthritis; Th17;
D O I
10.3389/fimmu.2020.623874
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Axial spondyloarthritis is a prevalent form of chronic arthritis which is related to psoriatic arthritis and skin psoriasis. TNF and IL-17A as well as IL-17F are key cytokines contributing to the pathobiology of this disease, as evidence by the therapeutic efficacy of inhibition of these factors. Despite the evidence that IL-23 acts as an upstream driver of Th17 cells, the T lymphocytes producing IL-17, and that IL-23 inhibition shows profound efficacy in psoriasis, blocking IL-23 failed to show any evidence of clinical efficacy in axial spondyloarthritis. In this viewpoint article, we revisit the reasons-to-believe in a role of IL-23 in the pathobiology of axial spondyloarthritis, discuss what we have learned on the pathobiology of this disease in general and on the function of the IL-23/IL-17 axis in particular, and share a handful of lessons learned that are of relevance for the translation of emerging biological insights into clinical therapeutics.
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页数:4
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