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Effect of Interferon- and Glucose on Major Histocompatibility Complex Class I and Class II Expression by Pancreatic ß- and Non-ß-Cells¹

Diabetes Research Center, Vrije Universiteit Brussel, 1090 Brussels, Belgium

Address all correspondence and requests for reprints to: Prof. D. Pipeleers, Department of Metabolism and Endocrinology, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium.

Surface major histocompatibility complex (MHC) class I and class II expression by pancreatic islet cells is considered a local initiator or regulator of immune processes that can lead to diabetes. Locally released cytokines, in particular interferon-, are known to stimulate MHC antigen expression by islet cells. The present study quantifies MHC expression in cultured pancreatic ß- and non-ß-cells from both rat and human organs. Interferon- increased MHC class I expression in endocrine ß- and non-ß-cells as well as in pancreatic ductal cells. The cytokine induced a 6-fold increase in the MHC class I messenger ribonucleic acid levels in pancreatic ß-cells; this effect was 2-fold amplified in the presence of elevated glucose levels (20 mmol/L instead of 6 mmol/L). No MHC class II expression was observed in endocrine ß- or non-ß-cells; human, but not rat, ductal cells exhibited MHC class II expression that increased in the presence of interferon-.

These data indicate that the increase in ß-cell MHC class I expression described in the pancreata of diabetic patients may result from stimulated transcription after exposure to locally released interferon- and/or to a hyperglycemic state. The association of human islets with ductal cells in which MHC class II expression is stimulated by interferon- makes these cells potential participants in the autoimmune process in diabetes.

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