IFN-tau suppresses both the autoreactive humoral and cellular immune responses and induces stable remission in mice with chronic experimental allergic encephalomyelitis.

We have previously shown that interferon-tau (IFN-tau) 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-tau is a type I IFN that has pregnancy recognition hormone activity in ruminants. Here we show that IFN-tau induced remission in SJL/J mice that had ongoing chronic active EAE disease and protected mice against secondary relapses. IFN-tau treatment reversed lymphocyte infiltration and microglial activation in the central nervous system. Mice that were treated with IFN-tau 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-tau either in vivo or in vitro blocked activation. Furthermore, IFN-tau inhibited MBP activation of T cells from EAE mice. Thus, IFN-tau inhibits the humoral arm as well as the cellular arm of the autoimmune disease EAE. The data presented here show that IFN-tau 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.