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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

Open Badges Oral presentation

Anti-TNF antibody therapy induces IL-17 suppressing regulatory T cells in patients with rheumatoid arthritis

Jenny McGovern*, Clare A Notley, Dao Nguyen, Claudia Mauri, David A Isenberg and Michael R Ehrenstein

  • * Corresponding author: Jenny McGovern

Author Affiliations

Division of Medicine, University College London, London WC1E 6JF, UK

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Arthritis Research & Therapy 2012, 14(Suppl 1):O42  doi:10.1186/ar3597

The electronic version of this article is the complete one and can be found online at:

Published:9 February 2012

© 2012 McGovern et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Oral presentation

Biologic therapies not only offer the prospect of improved patient outcomes in a variety of autoimmune diseases, but also the opportunity to explore the specific target's role in the underlying mechanisms of disease. Over recent years we have studied the role of regulatory T cells (Treg) in patients with rheumatoid arthritis before and after anti-TNF therapy. We have shown that Treg from patients with rheumatoid arthritis have defective suppressor function. This Treg defect is linked with abnormalities in the expression and function of CTLA-4. Anti-TNF antibody therapy did not reverse CTLA-4 dysfunction but instead induced the differentiation of a distinct and potent Treg population. These induced Treg were able to inhibit IL-17 production, in contrast to Treg from healthy individuals, patients with active RA or RA patients treated with etanercept, a modified TNF receptor. These results may provide mechanistic insight into the therapeutic benefit of switching between different anti-TNF agents and the differing incidence of tuberculosis between adalimumab and etanercept.