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Novel aspects of regulatory T cell dysfunction as a therapeutic target in giant cell arteritis
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  • Published on:
    How to improve Treg immune response in GCA? Comment on the paper of Adriawan et al.
    • Maxime SAMSON, MD, PhD Department of Internal Medicine and Clinical Immunology, Dijon University Hospital, F-21000 Dijon, France; Université Bourgogne
    • Other Contributors:
      • Hélène GREIGERT, MD
      • Marion CIUDAD, PhD student
      • Bernard BONNOTTE, MD, PhD

    We read with great interest the recently published article by Adriawan et al 1 in which the authors confirmed that the regulatory T response is deficient in GCA, which is related, at least in part, to a defect in the glycolytic pathway that yields to, a decrease in the expression of GARP and CD25 and a decrease in calcium influx after T-cell receptor engagement.
    Apart the fact that this study did not find a decrease in the percentage of circulating Treg, probably due to the small number of patients included compared to the other studies,2,3 these results confirm previous work in the field, including our own,3 and add new elements which provide a better understanding in the mechanistic pathways involved in this Treg dysfunction in GCA. The data from these 3 studies 1-3 suggest that interleukin-6, which is a major therapeutic target in GCA, plays a central role in the increase of FoxP3-exon 2 deficient (FoxP3∆2) Tregs, whose suppressive capacities are reduced, but which also induce an increase in IL-17 production because these cells produce more IL-17 than healthy Tregs and favour the Th17 polarization of effector CD4+ T cells.3
    In their work, the authors also showed that tocilizumab, by blocking IL-6 signaling, restores the calcium influx of Tregs and thus their suppressive function.1 This result is in agreement with our recently reported data showing that tocilizumab restored the ability of Tregs to inhibit effector T cell proliferation and Th17 polarization...

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    Conflict of Interest:
    Maxime SAMSON: Roche-Chugaï (travel fees, personnel fees for symposium and boards), Abbvie (consulting).
    Bernard BONNOTTE: Roche-Chugaï (board)