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Interferon beta induces interleukin‐10 expression: Relevance to multiple sclerosis
Author(s) -
Rudick Richard A.,
Ransohoff Richard M.,
Peppler Richard,
Medendorp Sharon Vanderbrug,
Lehmann Paul,
Alam John
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410400412
Subject(s) - multiple sclerosis , interferon , cytokine , beta (programming language) , immune system , medicine , interleukin , immunology , interferon beta 1b , interferon beta 1a , endocrinology , interferon beta , computer science , programming language
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 × 10 6 ‐IU than 6 × 10 6 ‐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.