Recombinant interferon-beta blocks proliferation but enhances interleukin-10 secretion by activated human T-cells

Results from recent clinical trials have indicated that recombinant interferon-beta (rIFN-beta) is a promising drug for the treatment of Multiple Sclerosis (MS), a disease of supposed autoimmune etiology. To gain insight into the immunoregulatory properties of this cytokine, we analyzed effects of interferon-beta (IFN-beta) on T-cell functions in vitro. Interferon-beta inhibited T-cell proliferation, as well as T-cell-dependent immunoglobulin secretion, in a dose-dependent manner. IFN-beta did not inhibit upregulations of CD40L on activated T-cells, but blocked induction of CD25 on stimulated T- and B-lymphocytes. Secretion of interferon-gamma (IFN-gamma), tumour necrosis alpha (TNF-alpha) and IL-13 was inhibited by the addition of IFN-beta, whereas IL-4 secretion was unaffected. Interestingly, IFN-beta enhanced secretion of IL-2 about two-fold and secretion of IL-10 nearly four-fold. In summary, these findings suggest that IFN-beta may exert direct effects on T- and beta-cell function in vivo. In addition, enhanced secretion of IL-10 by activated T-cells may interfere with newly initiated and ongoing inflammatory immune reactions.