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

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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.

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Correspondence to Jenny McGovern.

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Keywords

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