Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia
1996
The ability of interferon-α (IFN-α) to induce the adhesion molecules that characterize the
isletsof patients with type I diabetes has been investigated. We have found that all tested recombinant IFN-as will induce
major histocompatibility complex(
MHC)
class Ion 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 IIexpression 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
isletsof patients with type I diabetes. IFN-α is also produced in normal human
isletsduring 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-1in human
isletsand may also be a contributing factor to the failure of
isletgrafts.
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