Multiple Sclerosis Research Today is a free monthly online journal that collates and summarizes the latest research about Multiple Sclerosis, including details on diagnosis, symptoms, treatment, prognosis.

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

Buttmann M, Merzyn C, Rieckmann P

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

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.

Published 6 October 2004 in J Neuroimmunol, 156(1): 195-203.
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