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Original Articles

Very-Low-Dose Streptozotocin Induces Diabetes in Insulin Promoter-mB7-1 Transgenic Mice

  1. David M Harlan,
  2. Michelle A Barnett,
  3. Ryo Abe,
  4. Klaus Pechhold,
  5. Noelle B Patterson,
  6. Gary S Gray and
  7. Carl H June
  1. Immune Cell Biology Program, Naval Medical Research Institute Bethesda, Maryland
  2. Repligen Corporation Cambridge, Massachusetts
  1. Address correspondence and reprint requests to Dr. David M. Harlan, Immune Cell Biology Program, Naval Medical Research Institute, 8901 Wisconsin Ave., Bethesda, MD 20889-5607.
Diabetes 1995 Jul; 44(7): 816-823. https://doi.org/10.2337/diab.44.7.816
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Abstract

Transgenic mice that express mouse B7-1 (mB7-1, recently designated CD80) on their pancreatic β-cells maintain normal islet architecture, have normal pancreatic insulin content, and only rarely spontaneously develop insulitis and diabetes. Nevertheless, these mice display an extreme sensitivity to streptozotocin (STZ)-induced diabetes. Female mice were administered two STZ doses intraperitoneally, 20 and 40 mg/kg body wt, each for five consecutive days. Nontransgenic but otherwise syngeneic mice responded to the STZ with a moderate diminution in pancreatic insulin content but not with persistent glycosuria. In striking contrast, STZ administered to transgenic mice resulted in a severe diminution of pancreatic insulin content and in diabetes. Notably, the lower STZ dose resulted in diabetes only after a prolonged (26- to 100-day) latency. STZ-induced diabetes appears to be T-cell dependent, since treatment with T-cell–depleting (and in particular CD8+ subset-depleting) antibodies ameliorated the response. Anti-mB7-1 monoclonal antibody administration also prevented STZ-induced diabetes. Thus, unmasked mB7-1 is a required component in the pathway resulting in β-cell killing. Immunohistological analysis revealed that early after STZ administration, both mB7-1 transgenic and nontransgenic mice developed insulitis. While this insulitis resolved in the nontransgenic mice, the islet-infiltrating CD4+ and CD8+ T-cells in the transgenic mice were associated with complete β-cell destruction. These data suggest that STZ-induced diabetes in mB7-1 transgenic mice is an immune-mediated process with distinct potential advantages over existing insulindependent diabetes models.

  • Received January 3, 1995.
  • Revision received March 23, 1995.
  • Accepted March 23, 1995.
  • Copyright © 1995 by the American Diabetes Association

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July 1995, 44(7)
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Very-Low-Dose Streptozotocin Induces Diabetes in Insulin Promoter-mB7-1 Transgenic Mice
David M Harlan, Michelle A Barnett, Ryo Abe, Klaus Pechhold, Noelle B Patterson, Gary S Gray, Carl H June
Diabetes Jul 1995, 44 (7) 816-823; DOI: 10.2337/diab.44.7.816

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Very-Low-Dose Streptozotocin Induces Diabetes in Insulin Promoter-mB7-1 Transgenic Mice
David M Harlan, Michelle A Barnett, Ryo Abe, Klaus Pechhold, Noelle B Patterson, Gary S Gray, Carl H June
Diabetes Jul 1995, 44 (7) 816-823; DOI: 10.2337/diab.44.7.816
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