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Immunology and Transplantation

Humanized Mouse Model to Study Type 1 Diabetes

  1. Sandrine Luce1,2,
  2. Sophie Guinoiseau1,2,
  3. Alexis Gadault1,2,
  4. Franck Letourneur1,
  5. Bertrand Blondeau3,
  6. Patrick Nitschke2,
  7. Eric Pasmant2,4,
  8. Michel Vidaud4,
  9. François Lemonnier1,2 and
  10. Christian Boitard1,2⇑
  1. 1INSERM U1016, Institut Cochin, Paris, France
  2. 2Faculté de Médecine René Descartes, Université Paris Descartes, Paris, France
  3. 3INSERM U938, Centre de recherche Saint-Antoine, Paris, France
  4. 4Service de Biochimie et Génétique Moléculaire, Hôpital COCHIN, Paris, France
  1. Corresponding author: Christian Boitard, christian.boitard{at}aphp.fr.
Diabetes 2018 Sep; 67(9): 1816-1829. https://doi.org/10.2337/db18-0202
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Abstract

Key requirements in type 1 diabetes (T1D) are in setting up new assays as diagnostic biomarkers that will apply to prediabetes, likely T-cell assays, and in designing antigen-specific therapies to prevent T1D development. New preclinical models of T1D will be required to help with advancing both aims. By crossing mouse strains that lack either murine MHC class I and class II genes and insulin genes, we developed YES mice that instead express human HLA-A*02:01, HLA-DQ8, and insulin genes as transgenes. The metabolic and immune phenotype of YES mice is basically identical to that of the parental strains. YES mice remain insulitis and diabetes free up to 1 year of follow-up, maintain normoglycemia to an intraperitoneal glucose challenge in the long-term range, have a normal β-cell mass, and show normal immune responses to conventional antigens. This new model has been designed to evaluate adaptive immune responses to human insulin on a genetic background that recapitulates a human high-susceptibility HLA-DQ8 genetic background. Although insulitis free, YES mice develop T1D when challenged with polyinosinic-polycytidylic acid. They allow the characterization of preproinsulin epitopes recognized by CD8+ and CD4+ T cells upon immunization against human preproinsulin or during diabetes development.

Footnotes

  • This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db18-0202/-/DC1.

  • Received February 16, 2018.
  • Accepted June 15, 2018.
  • © 2018 by the American Diabetes Association.
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Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.

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Diabetes: 67 (9)

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September 2018, 67(9)
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Humanized Mouse Model to Study Type 1 Diabetes
Sandrine Luce, Sophie Guinoiseau, Alexis Gadault, Franck Letourneur, Bertrand Blondeau, Patrick Nitschke, Eric Pasmant, Michel Vidaud, François Lemonnier, Christian Boitard
Diabetes Sep 2018, 67 (9) 1816-1829; DOI: 10.2337/db18-0202

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Humanized Mouse Model to Study Type 1 Diabetes
Sandrine Luce, Sophie Guinoiseau, Alexis Gadault, Franck Letourneur, Bertrand Blondeau, Patrick Nitschke, Eric Pasmant, Michel Vidaud, François Lemonnier, Christian Boitard
Diabetes Sep 2018, 67 (9) 1816-1829; DOI: 10.2337/db18-0202
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  • Differentiating MHC-Dependent and -Independent Mechanisms of Lymph Node Stromal Cell Regulation of Proinsulin-Specific CD8+ T Cells in Type 1 Diabetes
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