Biological and clinical effects of anti-TNFalpha treatment

Autoimmun Rev. 2007 Nov;7(1):35-41. doi: 10.1016/j.autrev.2007.03.003. Epub 2007 Mar 26.


Tumor necrosis factor alpha (TNFalpha) is implicated in the pathogenesis of many chronic inflammatory diseases such as rheumatoid arthritis (RA), psoriasis and psoriatic arthritis (PsA), ankylosing spondylitis (AS), Crohn's disease, ulcerative colitis and uveitis. The availability of new pharmacological agents (infliximab, etanercept, adalimumab), able to selectively block the TNFalpha, has recently offered new opportunity for the treatment of these diseases. TNFalpha antagonists are different in the mechanism of action and are all effective agents in the treatment of RA and several chronic inflammatory diseases as a large number of controlled clinical trials have shown. Among biological effects of TNFalpha antagonists, the production of autoantibodies has been emphasized. This phenomenon is not correlated with the disease background, since anti-nuclear antibodies (ANA) and anti-double stranded-DNA antibodies (anti-dsDNA) induction is observed in RA as well as in spondyloarthritis (SpA) patients. Nonetheless, recent studies had reported a significant reduction in the serum titre of rheumatoid factor (RF) and/or anti-cyclic citrullinated peptide antibodies (anti-CCP) during anti-TNFalpha therapy. The TNFalpha antagonists represent a significant advance in the therapy of active RA and other chronic inflammatory diseases. However, they have distinct biological, clinical, and pharmacological properties that must be considered when selecting a drug for therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adalimumab
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
  • Antibodies, Monoclonal / immunology
  • Antibodies, Monoclonal / pharmacology
  • Antibodies, Monoclonal / therapeutic use
  • Antibodies, Monoclonal, Humanized
  • Antirheumatic Agents / pharmacology
  • Antirheumatic Agents / therapeutic use*
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / immunology
  • Autoantibodies / biosynthesis
  • Autoantibodies / blood
  • Chronic Disease
  • Etanercept
  • Humans
  • Immunoglobulin G / immunology
  • Immunoglobulin G / pharmacology
  • Immunoglobulin G / therapeutic use
  • Inflammation / drug therapy*
  • Inflammation / immunology
  • Infliximab
  • Receptors, Tumor Necrosis Factor / immunology
  • Receptors, Tumor Necrosis Factor / therapeutic use
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / immunology


  • Anti-Inflammatory Agents, Non-Steroidal
  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antirheumatic Agents
  • Autoantibodies
  • Immunoglobulin G
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Infliximab
  • Adalimumab
  • Etanercept