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

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

Mathias Buttmann  1 , Cornelia Merzyn, Peter Rieckmann
Affiliations
Comparative Study

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

Mathias Buttmann et al. J Neuroimmunol. 2004 Nov.

Abstract

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.

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