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Transgenic mice with I-A on islet cells are normoglycemic but immunologically intolerant
Insulin-dependent diabetes mellitus (IDDM) is caused by specific loss of the insulin-producing beta cells from pancreatic Langerhans islets. It has been proposed that aberrant expression of major histocompatibility complex (MHC) class II molecules on these cells could be a triggering factor for thei...
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Published in: | Science (American Association for the Advancement of Science) 1989-01, Vol.244 (4904), p.1179-1183 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Online Access: | Get full text |
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Summary: | Insulin-dependent diabetes mellitus (IDDM) is caused by specific loss of the insulin-producing beta cells from pancreatic Langerhans islets. It has been proposed that aberrant expression of major histocompatibility complex (MHC) class II molecules on these cells could be a triggering factor for their autoimmune destruction. This proposal was tested in transgenic mice that express allogeneic or syngeneic class II molecules on the surface of islet cells at a level comparable with the normally found on resting B lymphocytes. These animals do not develop diabetes, nor is lymphocyte infiltration of the islets observed. This immunological inactivity does not result from tolerance to the "foreign" class II molecules. |
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ISSN: | 0036-8075 |