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Correspondence
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. 1 Department of Internal Medicine and Clinical Immunology, François Mitterrand Hospital, Dijon University Hospital, Dijon, France
  2. 2 INSERM, 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

http://dx.doi.org/10.1136/annrheumdis-2017-211622

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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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    Footnotes

    • Contributors MS and TG did the experiments and collected data. SB included the patient. MS and BB wrote the manuscript.

    • Competing interests None declared.

    • Patient consent Obtained

    • Ethics approval The Institutional Review Board and the Ethics Committee of Dijon University Hospital.

    • Provenance and peer review Not commissioned; internally peer reviewed.

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