This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Weringer, E. J. Articles by Like, A. A. Search for Related Content PubMed PubMed Citation Articles by Weringer, E. J. Articles by Like, A. A.

American Journal of Pathology, Vol 132, 292-303, Copyright © 1988 by American Society for Investigative Pathology

REGULAR ARTICLES

Identification of T cell subsets and class I and class II antigen expression in islet grafts and pancreatic islets of diabetic BioBreeding/Worcester rats

EJ Weringer and AA Like
Department of Pathology, University of Massachusetts Medical School, Worcester 01655.

The BioBreeding/Worcester (BB/Wor) rat develops a spontaneous disorder that closely resembles human insulin-dependent (Type I) diabetes mellitus. The syndrome is preceded by lymphocytic insulitis that destroys pancreatic beta cells. The morphologic features of the spontaneous insulitis lesions are also observed within islets transplanted beneath the renal capsule of diabetes-prone and diabetic animals. This study reports the results of experiments in which immunohistochemical techniques were used to characterize the phenotype of the infiltrating mononuclear cells and detect the expression of class I and class II MHC antigens in native islets and islet transplants in diabetic and diabetes-prone BB/Wor rats. The infiltrates within native pancreatic islets and islet grafts were comprised predominantly of Ia+ cells (dendritic cells and macrophages) CD4+ cells (helper/inducer lymphocytes and macrophages), CD5+ (pan-T) cells and smaller numbers of CD8+ (cytotoxic/suppressor and NK) cells. Pancreatic and graft insulitis were accompanied by markedly enhanced class I antigen expression on islet and exocrine cells. Class II (Ia) antigens were not detected on normal islet cells, islets undergoing insulitis or on islet transplants subjected to immune attack. In islet grafts stained with polymorphic MAbs that distinguish Ia antigens of donor and host origin, Ia antigen expression was limited to infiltrating dendritic cells and macrophages of host origin. It is concluded that the phenotypes of infiltrating mononuclear cells that comprise the insulitis lesion in spontaneous BB/Wor diabetes, and the inflammatory attack on islets transplanted into diabetic BB/Wor rats are the same, that pancreatic islet and graft insulitis occur in the presence of enhanced class I antigen expression but in the absence of class II antigen expression, and that infiltrating Ia+ cells within islet grafts are exclusively of recipient (BB/Wor) origin and may explain the initiation of immune insulitis within grafts derived from donors of incompatible MHC.

This article has been cited by other articles:

				T. Hayashi and D. L. Faustman Role of Defective Apoptosis in Type 1 Diabetes and Other Autoimmune Diseases Recent Prog. Horm. Res., January 1, 2003; 58(1): 131 - 153. [Abstract] [Full Text] [PDF]

				T. Hayashi and D. Faustman NOD Mice Are Defective in Proteasome Production and Activation of NF-kappa B Mol. Cell. Biol., December 1, 1999; 19(12): 8646 - 8659. [Abstract] [Full Text] [PDF]