Tumor necrosis factor and granuloma biology: explaining the differential infection risk of etanercept and infliximab

Semin Arthritis Rheum. 2005 Apr;34(5 Suppl1):34-8. doi: 10.1016/j.semarthrit.2005.01.009.


Several studies show that the risk of granulomatous infections following therapy with the anti-tumor necrosis factor (TNF) antibody infliximab is higher than after treatment with the soluble TNFRp75 immunoglobulin fusion construct etanercept. Therefore, despite sharing a common target, it is possible that the actual mode of action of the 2 biologicals differs in vivo. TNF is known to participate in the induction and maintenance of protective granulomas at multiple steps, and evidence supporting a differential inhibition of TNF bioactivity and signaling by the 2 drugs is discussed.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / antagonists & inhibitors*
  • Antibodies, Monoclonal / adverse effects*
  • Etanercept
  • Granuloma / chemically induced*
  • Humans
  • Immunoglobulin G
  • Infections / chemically induced*
  • Infliximab
  • Receptors, Tumor Necrosis Factor / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*


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