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Effect of IL-17A blockade with secukinumab in autoimmune diseases
  1. Dhavalkumar D Patel1,
  2. David M Lee1,
  3. Frank Kolbinger1,
  4. Christian Antoni2
  1. 1Autoimmunity, Transplantation and Inflammation Disease Area, Novartis Institutes for BioMedical Research, Basel, Switzerland
  2. 2Integrated Hospital Care Franchise, Novartis Pharma AG, Basel, Switzerland
  1. Correspondence to Dr Dhavalkumar D Patel, Autoimmunity, Transplantation and Inflammation Disease Area, Novartis Institutes for BioMedical Research, Basel CH-4002, Switzerland; office.patel{at}novartis.com

Abstract

Genetic studies and correlative expression data in diseased tissues have pointed to the role of interleukin (IL)-17 and Th17 cells in the pathogenesis of autoimmune disorders such as psoriasis, inflammatory bowel disease and seronegative spondyloarthropathies. Th17 cells are known to produce the proinflammatory cytokine IL-17A as well as other effector cytokines, including IL-17F and IL-22. Recent research has demonstrated that IL-17A is also expressed by multiple lineages of the innate immune system, including mast cells, neutrophils, dendritic cells, γδ-T cells, macrophages and natural killer cells. It can thus be expected that the inhibition of IL-17A as a therapeutic target in autoimmune disease would exert different physiological effects than the suppression of Th17 cell activity. Early clinical data are now available on secukinumab (AIN457), a recombinant, highly selective, fully human monoclonal anti-IL-17A antibody of the IgG1/κ isotype, enabling a preliminary assessment of the effects of IL-17A inhibition in multiple autoimmune diseases. Rapid and sustained symptom reductions in psoriasis, rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis have been observed in secukinumab-treated patients, with no overt safety signals. In conjunction with studies using the humanised anti-IL-17A monoclonal antibody (mAb) ixekizumab (LY2439821) and the fully human anti-IL-17RA mAb brodalumab (AMG 827), the findings on secukinumab provide evidence for the role of IL-17A in the pathophysiology of autoimmune disease and suggest the potential value of targeting this cytokine.

  • Psoriatic Arthritis
  • Rheumatoid Arthritis
  • Autoimmune Diseases
  • Ankylosing Spondylitis
  • DMARDs (biologic)

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