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Journal of Histochemistry and Cytochemistry, Vol. 48, 761-768, June 2000, Copyright © 2000, The Histochemical Society, Inc.

ARTICLE

Expression of Pancreatic Islet MHC Class I, Insulin, and ICA 512 Tyrosine Phosphatase in Low-dose Streptozotocin-induced Diabetes in Mice

Zhanchun Lia, Lijun Zhaoa, Stellan Sandlerb, and F. Anders Karlssona
a Departments of Medical Sciences, Uppsala University, Uppsala, Sweden
b Medical Cell Biology, Uppsala University, Uppsala, Sweden

Correspondence to: F. Anders Karlsson, Dept. of Medical Sciences, Internal Medicine, University Hospital, S-751 85 Uppsala, Sweden. E-mail: anders.karlsson@medicin.uu.se

Activated immune cells contribute to the development of diabetes mellitus in multiple low-dose streptozotocin-treated mice. However, a role in the process for MHC Class I restricted T-cells remains a matter of debate. In this study, we examined by confocal microscopy the pancreatic expression of MHC Class I protein, insulin, and ICA 512 protein tyrosine phosphatase in C57BL/Ks mice given 40 mg/kg bw streptozotocin IP on 5 consecutive days. All animals were hyperglycemic from Day 7 and onwards. A loss of ICA 512 from the central portions of the islets was noted on Day 3. On Day 7, an increase in MHC Class I expression, confined primarily to immune cells in the exocrine pancreas and the periinsular areas, was detected. Later, several MHC class I/glucagon and some MHC class I/insulin double-positive cells were found. The insulitis was maximal on Day 14 and declined thereafter. The induction of MHC Class I expression in endocrine cells, occuring only after the cellular infiltration and when the animals were diabetic, indicates that the immune component of the disease does not depend on MHC Class I-restricted cytotoxic T-cells but rather comprises a non-antigen-specific process. (J Histochem Cytochem 48:761–767, 2000)

Key Words: diabetes, ICA 512, MHC class I, insulin, pancreatic islets, streptozotocin


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