Immunoregulatory effects of interferon-beta and interacting cytokines on human vascular endothelial cells. Implications for multiple sclerosis autoimmune diseases.
Experiments in which monocytes from normal subjects and MS patients were pre-treated in vitro with methylprednisolone prior to IFN-beta stimulation revealed that induction of HLA-DR was significantly inhibited; in contrast, IFN-beta induced HLA-DR expression was not down-regulated following subsequent in vitro treatment with methylprednisolone.
The clinical efficacy of interferon beta (IFN-beta) therapy in reducing exacerbations of relapsing-remitting MS has been related to antagonistic effects on various activities of IFN-gamma, including MHC-II gene induction.
We conclude that long-term cytokine modulation by IFNbeta-1a differs from acute effects and that downregulation of both pro- and anti-inflammatory cytokines, rather than a shift in the cytokine profile, is apparent after 6 months of IFNbeta-1a treatment of MS patients.
Whether the down-regulatory effects on pro-inflammatory and upregulatory effects on anti-inflammatory molecules are a direct result of IFN-beta on the immune system or secondary to clinical stabilization of MS pathology induced by IFN-beta remains to be evaluated.
We examined whether interferon-beta (IFN-beta) had the ability to regulate the production of chemokines and the expression of their receptors in T cells derived from patients with MS.
Thyroid dysfunction and autoimmunity have been reported during type I interferon therapy, namely interferon-alpha for chronic hepatitis or interferon-beta for multiple sclerosis.
Specifically, we addressed the effect of IFN-beta on T helper-1 differentiation- or lineage markers such as the IL-12 receptor beta2 chain and the chemokine receptor CCR5 that have been implicated in the pathogenesis of MS.
Previously, we have reported the development of a new quantitative-competitive polymerase chain reaction (qc-PCR) method to evaluate interferon-beta (IFNbeta) bioavailability in multiple sclerosis (MS) patients, by measuring mRNA of mixovirus resistance protein A (MxA).
To date, interferon-beta (IFN-beta) is the most effective and reliable therapy in the majority of MS patients, although the mechanisms underlying its therapeutic effects are not fully understood.
Seizures and extrapyramidal symptoms in a patient with Tourette's syndrome, Asperger's syndrome, and multiple sclerosis treated with interferon beta-1a and clomipramine.
Interferon-beta is thought to provide clinical improvement to multiple sclerosis (MS) patients, in part, through its ability to suppress the generation of IL-12-dependent autoimmune T helper type 1 (Th1) cells by monocyte-derived dendritic cells (DC).