Furthermore, ferucarbotran treatment increased the number of CD3<sup>+</sup>, Iba-1<sup>+</sup>, IL-6<sup>+</sup>, Iba-1<sup>+</sup>TNF-α<sup>+</sup> and CD3<sup>+</sup>IFN-γ<sup>+</sup> cells in the spinal cord of EAE mice.
In this work, we evaluated the sustained delivery of IFN-α1, either alone or fused to apolipoprotein A-1 by means of an adeno-associated viral (AAV) system in the mouse model of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.
Ablation of the IFN-α/β receptor (IFNAR) in astrocytes using mGFAPcre IFNAR<sup>fl/fl</sup> mice resulted in severe encephalomyelitis and mortality, coincident with uncontrolled virus replication.
Adoptive transfer of in vitro DMF-treated myelin peptide-reactive IL-17A<sup>low</sup> IFN-γ<sup>low</sup> IL-4<sup>+</sup> CD4<sup>+</sup> T cells prior to immunization for EAE reduces the severity of encephalomyelitis.
The results showed that SHED infusion ameliorated EAE clinical score with reduced number of infiltrating IFN-γ<sup>+</sup>CD8<sup>+</sup>, IL-4<sup>+</sup>CD8<sup>+</sup>, IFN-γ<sup>+</sup>CD4<sup>+</sup> and IL-4<sup>+</sup>CD4<sup>+</sup> T cells into the central nervous system (CNS).
IFN-β<sup>-/-</sup> DCs from mice immunized to develop EAE induce greater proliferation of MOG-transgenic CD4<sup>+</sup> T cells and promote interleukin-17 production by these T cells.
We found that treatment with CpG type A ODN (CpG-A), known to induce high amounts of IFN-<i>α</i> in pDCs, significantly reduced disease severity in EAE, relative to controls (12.63 ± 1.86 versus 23.49 ± 1.46, resp.; <i>p</i> = 0.001).
Purified IgG2a monoclonal anti-MOG antibody and mouse complement were stereotactically injected into the corpus callosum of wild-type and type I IFN receptor deficient mice (IFNAR1-KO) with and without pre-established experimental autoimmune encephalomyelitis (EAE).
The generation of type 1 IFN can be minimized by using polar, nonionizable, amyloidogenic peptides, which are effective in both Th1 and Th17 polarized EAE.
Resultant N-terminal truncated IFN mimetics functioned intracellularly as antivirals as well as therapeutics against experimental allergic encephalomyelitis without the undesirable side effects that limit the therapeutic efficacy of IFNβ in treatment of multiple sclerosis.
It can also amelioriate the development of experimental allergic encephalomyelitis (EAE) without the usual side effects of IFN therapy in mice autoimmunized with myelin basic protein.