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

被引：22

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

来源：

FRONTIERS IN IMMUNOLOGY | 2021年 / 11卷

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.

引用

页数：4