Interferon-beta induces transient systemic IP-10/CXCL10 chemokine release in patients with multiple sclerosis

J Neuroimmunol. 2004 Nov;156(1-2):195-203. doi: 10.1016/j.jneuroim.2004.07.016.


Reduction of chemokine expression induced by human recombinant Interferon (IFN)-beta is thought to be a therapeutic mechanism of its action in the treatment of multiple sclerosis (MS). In vitro, IFN-beta can induce chemokine expression. Here we show that a single injection of IFN-beta induced a transient strong increase of IP-10/CXCL10 and a weak elevation of MCP-1/CCL2 plasma levels in MS patients on continuing treatment with IFN-beta. IP-10/CXCL10 bursts, which were not observed in glatiramer acetate (GA)-treated patients, correlated with occurrence of flu-like symptoms. Systemic IP-10/CXCL10 release induced by IFN-beta may influence its therapeutic effect--either negatively or positively.

Publication types

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

MeSH terms

  • Adult
  • Chemokine CXCL10
  • Chemokines, CXC / metabolism*
  • Female
  • Humans
  • Interferon-beta / administration & dosage*
  • Interferon-beta / physiology
  • Male
  • Middle Aged
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / metabolism
  • Statistics, Nonparametric


  • CXCL10 protein, human
  • Chemokine CXCL10
  • Chemokines, CXC
  • Interferon-beta