Interferon beta in multiple sclerosis

Interferon beta 1B (IFN beta(1b)) lessens multiple sclerosis (MS) attack frequency and accumulating disease burden as assessed by MRI. The agent is an immune system modulator. The immune response in RIS is thought to involve a delayed-type hypersensitivity (DTH) response mediated by Th1 type T cells. IFN beta(1b) lessens expression of MHC-class II proteins on blood monocytes but only after a delay, This action could impede antigen presentation. Expression of the B7-1 costimulatory molecule on B cells is also reduced in RIS patients receiving IFN beta(1b), Downregulation of B7-1 expression could inhibit Th1 cell activation, IFN beta(1b) exerts an antiproliferative effect on T cells, an action which could lessen the magnitude of Th1 cell responses. Several cytokines are secreted by Th1 cells or by the monocytes/macrophages that they activate. IL-2, IFN-gamma, lymphotoxin, and tumor necrosis factor (TNF) are made by activated Th1 type T cells, IL-l, and TNF by activated macrophages. IFN beta(1b) increases IL-2 production in vitro but decreases production of IFN gamma, LT, and TNF. If these same effects occur in vivo, a substantial attenuation of the effector arm of DTH response would be anticipated. IFN beta(1b) has no known effect on Th2 type T cells. It increases CDS cell function including that of CD8 suppressor cells, the function of which is known to be deficient when MS is active. Production of the suppressive cytokines IL-10 and transforming growth factor beta-1 is increased in vitro by IFN beta(1b). Taken in sum, the immunomodulatory actions of IFN beta(1b) acting in concert would be expected to attenuate DTH responses and exert a beneficial effect in MS, as is found. (C) 1996 Academic Press, Inc.