The introduction of immunomodulatory therapy with interferon beta more than a decade ago was a major breakthrough in the treatment of multiple sclerosis (MS).1 Therapy with interferon beta includes 3 different preparations with proved therapeutic efficacy in relapsing-remitting MS and in secondary progressive MS with superimposed relapses. Inasmuch as the etiology of MS remains largely unknown and its pathogenesis is complex, it has been challenging to identify exactly the central mechanism of action of this therapeutic agent. There are numerous proposed mechanisms of action of interferon beta by which it is thought to mediate its beneficial effects.1 Interferon beta can influence antigen presentation by reducing the expression of major histocompatibility complex molecules and changing the expression pattern of costimulatory molecules.2 In addition, it can alter the cytokine and chemokine secretion patterns of immune cells, thereby inducing primarily noninflammatory mediators3 but also eliciting a transient increase in certain chemokines.4 Moreover, interferon beta can influence immune cell migration across biological barriers by changing the expression of adhesion molecules and matrix metalloproteinases, ameliorating blood-brain barrier dysfunction, and enhancing apoptotic elimination of activated T cells.1 Collectively, interferon beta seems to redress an immune balance that is disturbed on multiple levels, and the resulting biological net effect may underlie its clinical usefulness.
Hofstetter HH, Stüve O, Hartung H. Fine-tuning the Homeostasis of Regulatory T Cells: New Mechanism of Immunomodulatory Therapy in Multiple Sclerosis. Arch Neurol. 2008;65(11):1417–1418. doi:10.1001/archneur.65.11.1417
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