Abstract

 

Spondyloarthritis (SpA) is an umbrella term describing a family of chronic inflammatory rheumatic diseases. These diseases are characterised by inflammation of the axial skeleton, peripheral joints, and entheseal insertion sites throughout the body which can lead to structural joint damage including formation of axial syndesmophytes and peripheral osteophytes. Genetic evidence, preclinical and clinical studies indicate a clear role of interleukin (IL)- 23 and IL-17 as mediators in SpA pathogenesis. Targeting the IL-23/-17 pathways seems an efficient strategy for treatment of SpA patients, and despite the remaining challenges the pathway holds great promise for further advances and improved therapeutic opportunities. Much research is focusing on serological markers and imaging strategies to correctly diagnose patients in the early stages of SpA. Biomarkers may facilitate personalised medicine tailored to each patient's specific disease to optimise treatment efficacy and to monitor therapeutic response. This narrative review focuses on the IL-17 pathway in SpA-related diseases with emphasis on its role in pathogenesis, current approved IL-17 inhibitors, and the need for biomarkers reflecting core disease pathways for early diagnosis and measurement of disease activity, prognosis, and response to therapy.

Keywords: Biomarkers of inflammation and tissue remodelling including parameters of angiogenesis and autoantibodies are investigated to reflect core disease pathways for early diagnosis, measurement of disease activity, prognosis, and response to therapy in SpA.; IL-17 targeting therapies have shown to be effective in patients with SpA, which has expanded the number of treatment options beyond TNF inhibitor therapy; Limited data is available on the effect of IL-17 on radiographic progression, and much research is focusing on serological biomarkers including imaging strategies to better understand the effect of IL-17 inhibition; SpA is a heterogeneous disease built on inflammation, bone erosion and new bone formation arising through poorly understood mechanisms; Standard TNF inhibitor therapy improves symptoms, functional mobility and reduces disease activity, however, almost 40% of axSpA patients do not sufficiently respond to the anti-TNF treatment.

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