Autoimmunity and anti-TNF-α agents

Fabiola Atzeni, Maurizio Turiel, Franco Capsoni, Andrea Doria, Pierluigi Meroni, Piercarlo Sarzi-Puttini

Research output: Contribution to journalArticle

Abstract

Treatment of rheumatoid arthritis (RA) patients with anti-tumor necrosis factor-alpha (anti-TNF-α) biologic agents has been associated with a reduction in the levels of specific autoantibodies, such as rheumatoid factor (RF) and anticyclic citrullinated peptide (anti-CCP), and the induction of non-organ-specific autoantibodies (antinuclear antibodies [ANAs], anti-dsDNA, and antiphospholipid antibodies [aPLs]). The mechanisms by which the blockade of anti-TNF-α decreases the generation of specific autoantibodies, such as anti-CCP and RF, are not yet known. However, it has been shown that these agents can downregulate the production of several inflammatory cytokines and mediators and that these anti-inflammatory effects may account for reduced autoantibody generation, particularly in the synovial compartment. Infliximab treatment leads to the induction of ANAs in 63.8% of RA patients and 49.1% of Crohn's disease (CD) patients, and anti-dsDNA antibodies in 13% of RA patients and 21.5% of CD patients, respectively. The development of ANAs and anti-dsDNA antibodies has also been described after etanercept therapy in 11% and 15% of RA patients, respectively. In the controlled trials, increases in ANA and anti-dsDNA titers were observed in 5.3% and in 12.9% of adalimumab-treated RA patients. Only limited data on the induction of aPL antibodies during TNF-α blocking treatment are available.

Original languageEnglish
Pages (from-to)559-569
Number of pages11
JournalAnnals of the New York Academy of Sciences
Volume1051
DOIs
Publication statusPublished - 2005

Keywords

  • Adalimumab
  • Anticyclic citrullinated peptide antibodies (anti-CCP)
  • Autoantibodies
  • Autoimmunity
  • Etanercept
  • Infliximab
  • Rheumatoid factor

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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