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Diabetes, Vol 45, Issue 10 1336-1343, Copyright © 1996 by American Diabetes Association

ARTICLES

Control of islet intercellular adhesion molecule-1 expression by interferon-alpha and hypoxia

D Chakrabarti, X Huang, J Beck, J Henrich, N McFarland, RF James and TA Stewart
Department of Molecular Oncology, Genentech, Inc., South San Francisco, California 94080, USA.

The ability of interferon-alpha (IFN-alpha) to induce the adhesion molecules that characterize the islets of patients with type I diabetes has been investigated. We have found that all tested recombinant IFN-as will induce major histocompatibility complex (MHC) class I on arterial endothelial cells. Some but not all IFN-as will induce intercellular adhesion molecule-1 (ICAM-1). However, there is only a transient and modest increase in VCAM on arterial endothelial cells. IFN-alpha has very little effect on endothelial MHC class II expression but will induce these proteins on monocytes. Thus, there is a close concordance between the biological actions of IFN-alpha and the appearance of those adhesion molecules induced in the islets of patients with type I diabetes. IFN-alpha is also produced in normal human islets during short-term cultures, probably as a result of the ischemia present at the center of the islet. This induction of IFN-alpha by hypoxia may explain the previously reported spontaneous induction of ICAM-1 in human islets and may also be a contributing factor to the failure of islet grafts.
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Copyright © 1996 by the American Diabetes Association.