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Ustekinumab inhibits Th1 and Th17 polarisation in a patient with giant cell arteritis
  1. Maxime Samson1,2,
  2. Thibault Ghesquière2,
  3. Sabine Berthier1,
  4. Bernard Bonnotte1,2
  1. 1Department of Internal Medicine and Clinical Immunology, François Mitterrand Hospital, Dijon University Hospital, Dijon, France
  2. 2INSERM, UMR1098, University of Bourgogne Franche-Comté, FHU INCREASE, Dijon, France
  1. Correspondence to Pr Bernard Bonnotte, Department of Internal Medicine and Clinical Immunology, François Mitterrand Hospital, Dijon University Hospital, 21000 Dijon, France; bernard.bonnotte{at}chu-dijon.fr

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Although glucocorticoids (GC) remain the corner stone of giant cell arteritis (GCA) treatment, GC-sparing strategies are needed because GC are responsible for side effects.1 Recent advances in the pathophysiology of GCA showed that CD4+ T cells are recruited in the arterial wall and polarised into Th1 and Th17 cells,2 3 the latter being sensitive to GC-mediated suppression, whereas Th1 response persists in GC-treated patients,2 which triggers the recruitment of macrophages4 and could be implicated in the occurrence of relapses when GC are tapered. Interleukin (IL)-12 and IL-23 are two cytokines involved in Th1 and Th17 polarisations, respectively.5 These two cytokines share a common subunit (p40), which allows ustekinumab, a humanised anti-p40 monoclonal antibody, to target both IL-12 and IL-23 pathways, thus disrupting in theory Th1 and Th17 immune responses.6 Recently, an open-label study reported on the efficacy and safety of …

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