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Ingested type I interferon: state of the art as treatment for autoimmunity. Exp Biol Med (Maywood) 2002 Dec;227(11):981-8

Date

12/18/2002

Pubmed ID

12486207

DOI

10.1177/153537020222701105

Scopus ID

2-s2.0-0036913590   5 Citations

Abstract

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-alpha preserved residual beta-cell function in recent onset patients. In a second phase I trial, treatment of rheumatoid arthritis with ingested IFN-alpha 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-gamma production after ingesting IFN-alpha. In a phase II randomized, placebo-controlled, double-blind trial in multiple sclerosis, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. Tumor necrosis factor-alpha and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. Ingested IFN-alpha was not toxic in any of these clinical trials. These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity.

Author List

Brod SA

Author

Staley A. Brod MD Professor in the Neurology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Administration, Oral
Autoimmune Diseases
Clinical Trials as Topic
Humans
Interferon Type I