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Interleukin-17 Inhibitors for the Treatment of Ankylosing Spondylitis.

ABSTRACT: Tumor necrosis factor inhibitor (TNFi) has been applied in the treatment of ankylosing spondylitis (AS) for many years but still with an unmed need due to inefficacy or intolerance. Current treatment guideline recommended the use of IL-17 inhibitors over a second TNFi in patients with primary nonresponse to the first TNFi. We herein review the present available IL-17 inhibitors including secukinumab (SEC), ixekizumab (IXE), brodalumab and bimekizumab (BKZ) in clinical trials of AS. Therapeutic response and safe profile have been discussed in detail for each drug. Overall, IL-17 inhibitors were proved to be alternatives for biologic disease-modifying anti-rheumatic drugs (bDMARDs) in AS, which might be safer for tuberculosis while candida infection should be monitored in long term treatment.

SUBMITTER: Huang JX

PROVIDER: S-EPMC9524761 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Interleukin-17 Inhibitors for the Treatment of Ankylosing Spondylitis.

Huang Jin-Xian JX Zhang Li-Jun LJ Wei James Cheng-Chung JC

Rheumatology and immunology research 20201201 1

Tumor necrosis factor inhibitor (TNFi) has been applied in the treatment of ankylosing spondylitis (AS) for many years but still with an unmed need due to inefficacy or intolerance. Current treatment guideline recommended the use of IL-17 inhibitors over a second TNFi in patients with primary nonresponse to the first TNFi. We herein review the present available IL-17 inhibitors including secukinumab (SEC), ixekizumab (IXE), brodalumab and bimekizumab (BKZ) in clinical trials of AS. Therapeutic r ...[more]

PMID: 36465082

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Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling. Fifteen knee synovial biopsy tissue samples consisting of six seronegative spondyloarthropy (SpA), two ankylosing spondylitis (AS), three osteoarthritis (OA) and four normal control biopsies were obtained from the Synovial Tissue Bank at the Repatriation General Hospital in Adelaide, South Australia with the appropriate ethical approval (Supplementary Table 1). All patients provided informed written consent.

Dataset Information

Interleukin-17 Inhibitors for the Treatment of Ankylosing Spondylitis.

Publications

Interleukin-17 Inhibitors for the Treatment of Ankylosing Spondylitis.

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