Interferon-beta induces transient systemic IP-10/CXCL10 chemokine release in patients with multiple sclerosis.
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.
Clinical Research Unit for Multiple Sclerosis and Neuroimmunology, Department of Neurology, Julius-Maximilians-University, Josef-Schneider-Str. 11, D-97080 Würzburg, Germany. m.buttmann@mail.uni-wuerzburg.de
Mathias
M
Buttmann
Cornelia
C
Merzyn
Peter
P
Rieckmann
D000328:Adult; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000378:metabolism*; D005260:Female; D006801:Humans; D016899:Interferon-beta / Q000008:administration & dosage* / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000276:immunology* / Q000378:metabolism; D018709:Statistics, Nonparametric
C114753:CXCL10 protein, human; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D016899:Interferon-beta