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Abstract
Background: The modes of action of interferon beta (IFN-β) 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-β 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-β 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-γ. The enhancing effect of IFN-β 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-β inhibits the production of other cytokines, including tumor necrosis factor-α (TNF-α), IL-1β, IL-4, IL-12, and IL-13.
Conclusions: The increase of IL-10 in microglia–T cell interaction by IFN-β 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-β in MS.–1505
- Received March 24, 2000.
- Accepted June 25, 2000.
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