Abstract
Byline: Mustafa G. Mujtaba, Wolfgang J. Streit, Howard M. Johnson We have previously shown that interferon-I (IFN-I) pretreatment inhibits the development of both acute and chronic mouse experimental allergic encephalomyelitis (EAE), an animal model for the human demyelinating disease multiple sclerosis (MS). IFN-I is a type I IFN that has pregnancy recognition hormone activity in ruminants. Here, we show that IFN-I induced remission in SJL/J mice that had ongoing chronic active EAE disease and protected mice against secondary relapses. IFN-I treatment reversed lymphocyte infiltration and microglial activation in the central nervous system. Mice that were treated with IFN-I had lower levels of anti-MBP antibodies than untreated mice in both chronic and acute forms of EAE. MBP induced proliferation in B cells from EAE mice, but treatment with IFN-I eitherin vivoorin vitroblocked activation. Furthermore, IFN-I inhibited MBP activation of T cells from EAE mice. Thus, IFN-I inhibits the humoral arm as well as the cellular arm of the autoimmune disease EAE. The data presented here show that IFN-I inhibits both B cell and T cell responses in EAE as well as active, chronic EAE, and this may help explain the effectiveness of type I IFNs in treatment of MS. Article History: Received 5 January 1998; Accepted 3 April 1998 Article Note: (footnote) [star] This research was supported by Grants CA69959 and R37AI25904 from the National Institutes of Health. This article is Florida Agriculture Experiment Station Journal Series R-06324.