The ability of interferon-α (IFN-α) 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-α 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-α and the appearance of those adhesion molecules induced in the islets of patients with type I diabetes. IFN-α 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-α 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.
Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia
Debasis Chakrabarti, Xiaojian Huang, Joanne Beck, Jill Henrich, Nancy McFarland, Roger F L James, Timothy A Stewart; Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia. Diabetes 1 October 1996; 45 (10): 1336–1343. https://doi.org/10.2337/diab.45.10.1336
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