S. Chabot et Vw. Yong, Interferon beta-1b increases interleukin-10 in a model of T cell-microgliainteraction - Relevance to MS, NEUROLOGY, 55(10), 2000, pp. 1497-1505
Background: The modes of action of interferon beta (IFN-beta) 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-beta 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-beta potentiates the production
of IL-10 when they interact with adult human microglia, human fetal microg
lia, or U937 cells treated with phorbol-12-myristate-13-acetate (PMA) and I
FN-gamma. The enhancing effect of IFN-beta on IL-10 requires cell-cell cont
act, 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-beta
inhibits the production of other cytokines, including tumor necrosis facto
r-alpha (TNF-alpha), IL-1 beta, IL-4, IL-12, and IL-13. Conclusions: The in
crease of IL-10 in microglia-T cell interaction by IFN-beta together with a
decrease of other cytokines may lead to a noninflammatory milieu in the CN
S. This mechanism could contribute to the efficacy of IFN-beta in MS.