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Related Experiment Videos

I-E+ nonobese diabetic mice develop insulitis and diabetes

P L Podolin1, A Pressey, N H DeLarato

  • 1Department of Autoimmune Diseases Research, Mercke Research Laboratories, Rahway, New Jersey 07065.

The Journal of Experimental Medicine
|September 1, 1993
PubMed
Summary

Type I diabetes development in nonobese diabetic (NOD) mice depends on major histocompatibility complex (MHC) genes. Introducing non-NOD MHC, even with I-E expression, did not fully prevent diabetes, highlighting other protective genes.

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Area of Science:

  • Immunology
  • Genetics
  • Endocrinology

Background:

  • Type I diabetes in nonobese diabetic (NOD) mice is genetically controlled, with links to the major histocompatibility complex (MHC).
  • Previous studies showed that expressing an I-E transgene in NOD mice protects against insulitis and diabetes.

Purpose of the Study:

  • To investigate the impact of expressing I-E-positive (I-E+) or I-E-negative (I-E-) non-NOD MHC on the NOD background.
  • To determine the role of MHC-linked genes in diabetes development in NOD mice.

Main Methods:

  • Development of NOD MHC congenic strains expressing I-E+ or I-E- non-NOD MHC.
  • Crossing congenic strains with NOD mice to create F1 hybrids with mixed MHC.
  • Monitoring insulitis and diabetes incidence in congenic and F1 mice, including cyclophosphamide-induced diabetes models.

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Main Results:

  • NOD MHC congenic strains lacking the NOD MHC did not develop diabetes, indicating its necessity.
  • F1 mice with one dose of non-NOD MHC showed partial protection, but a proportion developed insulitis and diabetes.
  • I-E expression alone was insufficient to prevent diabetes; I-E- F1 strains were similarly protected as I-E+ F1 strains, suggesting other MHC-linked genes are crucial.

Conclusions:

  • Diabetes development in NOD mice requires the NOD MHC.
  • Non-NOD MHC-linked genes, independent of I-E expression, play a significant role in diabetes protection.
  • Thymic expression of non-NOD MHC is insufficient for protection without bone marrow-derived cell expression.