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Prevention of type-i diabetes in nonobese diabetic mice by virus-infection

Academic Article
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Overview

authors

  • Oldstone, Michael

publication date

  • January 1988

journal

  • Science  Journal

abstract

  • The nonobese diabetic (NOD) mouse is an animal model of type I diabetes and develops a characteristic autoimmune lesion in the islets of Langerhans with lymphocytic infiltration and destruction of pancreatic beta cells. The result is hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Diabetes usually begins by the sixth month of age but can occur earlier when young NOD mice are infused with lymphocytes from older NOD donors. When newborn or adult NOD mice were infected with a lymphotropic virus they did not become diabetic. The interaction between viruses and lymphocytes is pivotal in aborting diabetes, as established by experiments in which lymphocytes from virus-infected donors failed to transfer diabetes. In contrast, lymphocytes from age- and sex-matched uninfected donors caused disease. Therefore, viruses and, presumably, their products can be developed to be beneficial and may have potential as a component for treatment of human diseases. Further, these results point to the utility of viruses as probes for dissecting the pathogenesis of a nonviral disease.

subject areas

  • Animals
  • Autoimmune Diseases
  • Bone Marrow
  • Diabetes Mellitus, Experimental
  • Diabetes Mellitus, Type 1
  • Female
  • Islets of Langerhans
  • Lymphocyte Transfusion
  • Lymphocytes
  • Lymphocytic Choriomeningitis
  • Mice
  • Spleen
  • T-Lymphocytes
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Identity

International Standard Serial Number (ISSN)

  • 0036-8075

Digital Object Identifier (DOI)

  • 10.1126/science.3277269

PubMed ID

  • 3277269
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Additional Document Info

start page

  • 500

end page

  • 502

volume

  • 239

issue

  • 4839

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