IL-17 Inhibition in Axial Spondyloarthritis

Abhijeet Danve, Atulya (Atul) Deodhar

Research output: Contribution to journalReview article

Abstract

Axial spondyloarthritis (axSpA) affects 0.5–1.5�% of western population. Although TNF inhibitor (TNFi) medications have dramatically improved the treatment of this disabling disease, there are almost 40�% of patients who do not respond or have intolerance to TNFi. Several genetic, animal model, translational, and clinical studies have confirmed the role of IL-23/IL-17 pathway in the pathogenesis of the�axSpA. This axis could be targeted upstream by inhibiting either IL-23 or IL-23 receptor (IL-23R) or downstream by blocking IL-17 or IL-1RA receptor. Ustekinumab, a monoclonal antibody against p40 subunit of IL-12 and IL-23, and secukinumab, a monoclonal antibody against IL-17, have both demonstrated significant beneficial effect in controlling the disease activity, quality of life, and physical function as well as MRI scores in axSpA. Combined IL-17 and TNF-α blockade is a novel option for the patients with axSpA, which needs to be investigated further. We need prospective trials to evaluate the effect of IL-23/IL-17 axis manipulation on the radiographic progression and also on the extra-articular manifestations of axSpA.

Original languageEnglish (US)
Pages (from-to)221-230
Number of pages10
JournalCurrent Treatment Options in Rheumatology
Volume1
Issue number2
DOIs
StatePublished - Jun 1 2015

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Interleukin-23
Interleukin-17
Monoclonal Antibodies
Genetic Models
Interleukin-12
Animal Models
Joints
Quality of Life
Population

Keywords

  • Ankylosing spondylitis
  • Axial spondyloarthritis
  • Interleukin-17
  • Interleukin-17 inhibitors
  • Interleukin-23
  • Secukinumab
  • Th17 cells
  • Ustekinumab

ASJC Scopus subject areas

  • Rheumatology
  • Immunology and Allergy
  • Immunology

Cite this

IL-17 Inhibition in Axial Spondyloarthritis. / Danve, Abhijeet; Deodhar, Atulya (Atul).

In: Current Treatment Options in Rheumatology, Vol. 1, No. 2, 01.06.2015, p. 221-230.

Research output: Contribution to journalReview article

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