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Research Article Free access | 10.1172/JCI2899

IFN-gamma action on pancreatic beta cells causes class I MHC upregulation but not diabetes.

H E Thomas, J L Parker, R D Schreiber, and T W Kay

Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia.

Find articles by Thomas, H. in: PubMed | Google Scholar

Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia.

Find articles by Parker, J. in: PubMed | Google Scholar

Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia.

Find articles by Schreiber, R. in: PubMed | Google Scholar

Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia.

Find articles by Kay, T. in: PubMed | Google Scholar

Published September 15, 1998 - More info

Published in Volume 102, Issue 6 on September 15, 1998
J Clin Invest. 1998;102(6):1249–1257. https://doi.org/10.1172/JCI2899.
© 1998 The American Society for Clinical Investigation
Published September 15, 1998 - Version history
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Abstract

We have generated transgenic nonobese diabetic (NOD) mice expressing dominant negative mutant IFN-gamma receptors on pancreatic beta cells to investigate whether the direct effects of IFN-gamma on beta cells contribute to autoimmune diabetes. We have also quantitated by flow cytometry the rise in class I MHC on beta cells of NOD mice with increasing age and degree of islet inflammatory infiltrate. Class I MHC expression increases gradually with age in wild-type NOD mice; however, no such increase is observed in the transgenic beta cells. The transgenic mice develop diabetes at a similar rate to that of wild-type animals. This study dissociates class I MHC upregulation from progression to diabetes, shows that the rise in class I MHC is due to local IFN-gamma action, and eliminates beta cells as the targets of IFN-gamma in autoimmune diabetes.

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