Interferon beta induces interleukin‐10 expression: Relevance to multiple sclerosis

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Abstract
Interferon‐β decreases the relapse rate, relapse severity, progression of neurological disability, and development of new brain lesions observed with brain magnetic resonance imaging in relapsing‐remitting multiple sclerosis patients. The mechanism of action of this effect is presently unknown. This study was based on the hypothesis that immunoregulatory effects of interferon‐β may underlie its demonstrated clinical efficacy. The objective of the study was to determine the effect of interferon‐β‐1a on the expression of interleukin‐10, a cytokine that strongly inhibits cell‐mediated immune responses. Interferon‐β‐1a induced accumulation of interleukin‐10 messenger RNA and protein secretion by cultured peripheral blood mononuclear cells. The observed in vitro effects were similar for healthy control subjects and multiple sclerosis patients. Intramuscular injections of interferon‐β‐1a increased serum levels of interleukin‐10 at 12 and 24 hours following the injection. Greater increases were induced with 12 × 106‐IU than 6 × 106‐IU injections. The effect of interferon‐β‐1a was relatively specific for interleukin‐10, as treatment with interferon‐β‐1a did not result in accumulation of transforming growth factor‐β messenger RNA. Upregulation of interleukin‐10 represents a possible mechanism of action of interferon‐β's therapeutic effect in relapsing‐remitting multiple sclerosis, and has implications for therapy of other autoimmune diseases.