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From the Departments of Oncology (Dr. Yong) and Clinical Neurosciences (Drs. Chabot and Yong), University of Calgary, Alberta, Canada.
Address correspondence and reprint requests to Dr. V. Wee Yong, Departments of Oncology and Clinical Neurosciences, University of Calgary, 3330 Hospital Drive, NW, Calgary, Alberta T2N 4N1, Canada; e-mail: vyong{at}ucalgary.ca
BACKGROUND: The modes of action of interferon beta (IFN-ß) in MS remain unclear, but enhanced levels of the anti-inflammatory cytokine interleukin-10 (IL-10) in the CSF of patients with MS may be a marker of its prognostic efficacy.
OBJECTIVE: To examine potential mechanisms by which IL-10 may be increased by IFN-ß in the milieu of the CNS.
METHODS: A model of T cell interaction with microglia in vitro was used. Production of cytokines was monitored by measuring the levels of various cytokine proteins, using ELISA.
RESULTS: Pretreatment of T cells with IFN-ß potentiates the production of IL-10 when they interact with adult human microglia, human fetal microglia, or U937 cells treated with phorbol-12-myristate-13-acetate (PMA) and IFN-
. The enhancing effect of IFN-ß on IL-10 requires cell–cell contact, but does not seem to depend on pathways implicated in microglia–T cell interactions, involving CD40, CD23, and B7. In contrast to IL-10, IFN-ß inhibits the production of other cytokines, including tumor necrosis factor-
(TNF-), IL-1ß, IL-4, IL-12, and IL-13.
CONCLUSIONS: The increase of IL-10 in microglia–T cell interaction by IFN-ß together with a decrease of other cytokines may lead to a noninflammatory milieu in the CNS. This mechanism could contribute to the efficacy of IFN-ß in MS.–1505
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