Novel aspects of regulatory T cell dysfunction as a therapeutic target in giant cell arteritis
Compose Response

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g.
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests


  • A rapid response is a moderated but not peer reviewed online response to a published article in a BMJ journal; it will not receive a DOI and will not be indexed unless it is also republished as a Letter, Correspondence or as other content. Find out more about rapid responses.
  • We intend to post all responses which are approved by the Editor, within 14 days (BMJ Journals) or 24 hours (The BMJ), however timeframes cannot be guaranteed. Responses must comply with our requirements and should contribute substantially to the topic, but it is at our absolute discretion whether we publish a response, and we reserve the right to edit or remove responses before and after publication and also republish some or all in other BMJ publications, including third party local editions in other countries and languages
  • Our requirements are stated in our rapid response terms and conditions and must be read. These include ensuring that: i) you do not include any illustrative content including tables and graphs, ii) you do not include any information that includes specifics about any patients,iii) you do not include any original data, unless it has already been published in a peer reviewed journal and you have included a reference, iv) your response is lawful, not defamatory, original and accurate, v) you declare any competing interests, vi) you understand that your name and other personal details set out in our rapid response terms and conditions will be published with any responses we publish and vii) you understand that once a response is published, we may continue to publish your response and/or edit or remove it in the future.
  • By submitting this rapid response you are agreeing to our terms and conditions for rapid responses and understand that your personal data will be processed in accordance with those terms and our privacy notice.
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.

Vertical Tabs

Other responses

Jump to comment:

  • 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...

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