Drug-induced autoimmunity

Curr Opin Rheumatol. 2009 Sep;21(5):547-51. doi: 10.1097/BOR.0b013e32832f13db.


Purpose of review: This review aims to draw attention to the increased spectrum of the features of drug-induced autoimmunity (DIA), including both clinical and autoantibody profiles in addition to the potential chronicity of the syndrome.

Recent findings: In recent years, not only has the number of medications causing DIA increased but the spectrum of the features has broadened as well. With the use of newer medications, especially biologics, mostly directed towards immune system manipulation, the range of signs and symptoms of DIA as well as the patterns of autoantibody profiles have widened. Rashes and visceral involvement have started to be reported more often, especially with tumor necrosis factor antagonists. In addition, autoantibodies such as antidouble-stranded DNA, which are usually seen with idiopathic systemic lupus erythematosus, are appearing in place of the antihistone antibodies, typically found in drug-induced lupus. Finally, some medications have been implicated in causing the very same entity, which they may be used to treat. It is clear that progress in the field of pharmacogenetics and pharmacogenomics will help further our understanding of these and other adverse effects of medications.

Summary: Even though DIA has been known for many years, the underlying mechanisms remain unclear. However, with recently described new and unexpected features, novel hypotheses have been proposed, thus opening doors to further research in understanding these mechanisms.

Publication types

  • Review

MeSH terms

  • Autoantibodies / metabolism
  • Autoimmune Diseases / chemically induced*
  • Autoimmune Diseases / immunology
  • Autoimmunity / drug effects*
  • HLA Antigens
  • Humans
  • Lupus Erythematosus, Systemic / chemically induced
  • Lupus Erythematosus, Systemic / immunology
  • T-Lymphocytes, Helper-Inducer / drug effects
  • T-Lymphocytes, Helper-Inducer / immunology
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Vasculitis / chemically induced
  • Vasculitis / immunology


  • Autoantibodies
  • HLA Antigens
  • Tumor Necrosis Factor-alpha