Skip to content


  • Oral presentation
  • Open Access

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

  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Arthritis Research & Therapy201214 (Suppl 1) :O42

  • Published:


  • Rheumatoid Arthritis
  • Tuberculosis
  • Etanercept
  • Adalimumab
  • Specific Target

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.

Authors’ Affiliations

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


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

This article is published under license to 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.