The biology of TNF blockade

Arun G. Suryaprasad, Thomas P Prindiville

Research output: Contribution to journalArticle

89 Scopus citations

Abstract

Rheumatoid arthritis and Crohn's disease are costly diseases that result in significant long-term patient disability. They are chronic inflammatory diseases that are associated with increased production of Tumor Necrosis Factor (TNF). Blockage of this cytokine with bio-engineered compounds has significantly changed therapy of these diseases and has ushered in the era of biological therapy. The pro-inflammatory role of TNF is mediated by its essential respiratory burst function that is effectively inhibited by anti-TNF therapy. Anti-TNF therapy is effective in approximately two-thirds of patients to whom it is administered, but the effect is temporary. Lack of response to anti-TNF therapy stems from interplay of host-factors including: host cytokine response, disease phenotype, and antibody response to the anti-TNF agents. NOD 2, a defect present in approximately 50% of Crohn's disease patients, bears no relationship to non-response. Additionally, TNF promoter gene polymorphisms and TNF receptor gene heterogeneity play a significant role in non-response and disease course/severity. Adverse effects of anti-TNF therapy include early and delayed hypersensitivity reactions, cell-mediated infections, lupus-like syndrome, demyelinating diseases, and exacerbation of CHF.

Original languageEnglish (US)
Pages (from-to)346-357
Number of pages12
JournalAutoimmunity Reviews
Volume2
Issue number6
DOIs
StatePublished - Oct 2003

Keywords

  • Adalimumab
  • Anakina
  • Biologic therapy
  • Clinical trials
  • Crohn's disease
  • Etanercept
  • FoxP3
  • Gene polymorphism
  • Infliximab
  • NOD2
  • Remicade
  • Rheumatoid arthritis
  • TNF
  • TNF promoter
  • TNF receptor

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

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