More MS news articles for Feb 2002

Interferon-[beta] therapy for multiple sclerosis induces reciprocal changes in interleukin-12 and interleukin-10 production

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11835372&dopt=Abstract

Ann Neurol 2002 Feb;51(2):165-174
Byrnes AA, McArthur JC, Karp CL.
Department of Medicine, Johns Hopkins University Schools of Medicine and Public Health, Baltimore, MD.

Interleukin-12 is critical to the pathogenesis of experimental autoimmune encephalomyelitis in multiple species.

Interleukin-10, a dominant endogenous inhibitor of interleukin-12, is largely protective in these experimental surrogates for multiple sclerosis.

Such data have suggested that an interleukin-12/interleukin-10 immunoregulatory circuit is a key determinant of disease expression in experimental autoimmune encephalomyelitis.

For multiple sclerosis itself, compatible cytokine data have been reported.

The mechanisms underlying the beneficial effects of interferon-[beta] in multiple sclerosis remain unclear, hampering the search for more effective therapies. Of note, interferon-[beta] has reciprocal effects on these cytokines in vitro, suppressing interleukin-12 and augmenting interleukin-10 production.

To examine the effects of interferon-[beta] on the interleukin-12/interleukin-10 axis in multiple sclerosis, we characterized the production of these cytokines by peripheral blood mononuclear cells from patients beginning therapy with interferon-[beta].

Before therapy, multiple sclerosis patients exhibited increased stimulatable interleukin-12 production compared with controls.

Interferon-[beta] therapy leads to inhibition of interleukin-12 and augmentation of interleukin-10 production, significantly elevating the ratio of secreted interleukin-10 to interleukin-12.

These effects, observed equally in patients with relapsing-remitting and progressive disease, indicate that interferon-[beta] affects the interleukin-12/interleukin-10 axis in ways thought to be beneficial to multiple sclerosis patients.

More specific therapeutic targeting of these pathways may be warranted.