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MINIREVIEW

Ingested Type I Interferon: State of the Art as Treatment for Autoimmunity

Multiple Sclerosis Research Group, Department of Neurology, Graduate School of Biomedical Sciences in Immunology, University of Texas Health Science Center at Houston, Houston, Texas 77030

We have proposed a unifying hypothesis of the etiopathogenesis of autoimmunity that defines autoimmunity as a type I interferon (IFN) immunodeficiency syndrome. We have examined toxicity and potential efficacy in three phase I (type 1 diabetes, rheumatoid arthritis, multiple sclerosis) and one phase II clinical trials in multiple sclerosis. In a phase I open-label trial in type 1 diabetes, ingested IFN- preserved residual ß-cell function in recent onset patients. In a second phase I trial, treatment of rheumatoid arthritis with ingested IFN- reduced the secretion of interleukin (IL)-1, a pro-inflammatory cytokine. In a third phase I trial in multiple sclerosis, there was a significant decrease in peripheral blood mononuclear cell IL-2 and IFN- production after ingesting IFN-. In a phase II randomized, placebo-controlled, double-blind trial in multiple sclerosis, 10,000 IU ingested IFN- significantly decreased gadolinium enhancements compared with the placebo group at month 5. Tumor necrosis factor- and IFN- cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN- on decreasing gadolinium enhancements. Ingested IFN- was not toxic in any of these clinical trials. These studies suggest that ingested IFN- may have a potential role in the treatment of autoimmunity.

Key Words: autoimmunity • multiple sclerosis • type 1 diabetes • type I interferon • GALT • protein ingestion