Interferon beta induces T-helper 2 immune deviation in MS

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Abstract
Objective: To define the in vitro effects of interferon beta 1a (IFN-β1a) on myelin basic protein (MBP)-reactive T cells and to determine its regulatory mechanism on cytokine networks in patients with MS. Methods: The proliferation and cytokine production of MBP-reactive T-cell clones were measured in thymidine uptake assays and ELISA respectively. The precursor frequency of MBP-reactive T cells was estimated in a microwell culture system. Results: IFN-β inhibited the proliferation of established MBP-reactive T-cell clones, which correlated with enhanced production of anti-inflammatory interleukin (IL)-4 and IL-10, and a decrease in tumor necrosis factor alpha (TNF-α) and IFN-γ. When examined with peripheral blood mononuclear cells (PBMCs), IFN-β was found to reduce the in vitro T-cell responses to MBP, as indicated by the significantly decreased frequency of MBP-reactive T cells. The decreased frequency of MBP-reactive T cells corresponded to an augmented production of IL-4 and IL-10. Although the level of TNF-α and IFN-γ was generally unaltered or decreased, IFN-β appeared to enhance the production of IFN-γ in PBMCs derived from some individuals with MS. Conclusion: Interferon beta 1a (IFN-β) suppresses myelin basic protein (MBP)-reactive T cells and induces immune deviation toward the production of T-helper 2 cytokines, which may contribute to its therapeutic benefit in MS. The study also suggests some heterogeneity in MBP-reactive T-cell responses to IFN-β in different individuals with MS.

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