NOD mouse

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The NOD mouse ( English Non-Obese Diabetic Mouse ) is an inbred strain of the color mouse ( Mus musculus ) which, due to a high incidence of spontaneously occurring diabetes mellitus, is used in experimental diabetes research as an animal model for insulin-dependent type 1 diabetes is used. It was first described in 1980 and goes back to experiments at Shionogi in Japan , whose original goal was to breed mice with increased susceptibility to cataracts . Corresponding studies have shown that diabetes in the NOD mouse is caused by autoimmune processes and thus has similarities in terms of its etiology to insulin-dependent type 1 diabetes in humans , which occurs particularly in adolescence .

As with the human type 1 diabetes the diabetes of NOD mouse goes before the onset of the disease as insulitis called inflammatory infiltration of cells of the immune system in the islets of Langerhans of the pancreas (pancreatic) requires that leads to destruction of the insulin-producing beta cells . Genes in the main histocompatibility complex are the most important genetic risk markers of the disease in both the NOD mouse and man. Another similarity between type 1 diabetes in humans and diabetes in NOD mice is the occurrence of specific autoantibodies that are directed against antigens in the islet cells . The onset of the disease occurs in the NOD mouse from the 14th week of life. The incidence of diabetes is 60 to 80 percent for females and 20 to 30 percent for males, depending on the colony and housing conditions. In addition to susceptibility to diabetes, the NOD mouse also shows an increased incidence of other autoimmune diseases such as autoimmune thyroiditis , polyneuropathy and an SLE-like disease . In addition, autoimmune hepatitis , so-called experimental murine autoimmune hepatitis (emAIH), can also be induced in NOD mice .

In experimental diabetes research, the NOD mouse is, alongside the BB rat, the dominant animal model for human type 1 diabetes, in particular with regard to immunological and genetic aspects and for the investigation of new approaches to the prevention and therapy of the disease. NOD mouse diabetes differs from type 1 diabetes in humans primarily in the gender-specific differences in the incidence of the disease and in the comparatively mild course of diabetic ketoacidosis . In addition to the main NOD strain, the NOD / SCID mouse, which does not have an adaptive immune system , and the NOD / BDC-2.5 mouse, which carries a transgenic T-cell receptor against an antigen of the pancreas, are of particular importance experimental diabetes research .

literature

  • Edward H. Leiter, Michal Prochazka, Douglas L. Coleman: The Non-Obese Diabetic (NOD) Mouse. In: The American Journal of Pathology . 128 (2) / 1987, pp. 380-383.
  • Mark S. Anderson, Jeffrey A. Bluestone : The NOD Mouse: A Model of Immune Dysregulation. In: Annual Review of Immunology . 23/2005, pp. 447-485.
  • John P. Mordes, David V. Serreze, Dale L. Greiner, Aldo A. Rossini: Nonobese Diabetic Mice. In: Derek LeRoith, Simeon I. Taylor, Jerrold M. Olefsky: Diabetes mellitus: A Fundamental and Clinical Text. 3. Edition. Lippincott Williams & Wilkins, Philadelphia 2004, ISBN 0-7817-4097-5 , pp. 598-603
  • Li Zhang, George Eisenbarth : Immunopathogenesis of the NOD Mouse. In: George S. Eisenbarth: Immunoendocrinology: Scientific and Clinical Aspects. Springer, New York and London 2010, ISBN 1-60327-477-4 , pp. 199-214

Individual evidence

  1. ↑ Matthias Hardtke-Wolenski, Katja Fischer, Fatih Noyan, Jerome Schlue, Christine S. Falk, Maike Stahlhut, Norman Woller, Florian Kuehnel, Richard Taubert, Michael P. Manns, Elmar Jaeckel: Genetic predisposition and environmental danger signals initiate chronic autoimmune hepatitis driven by CD4 + T cells . In: Hepatology . tape 58 , no. 2 , August 2013, p. 718 ( PDF DOI = 10.1002 / hep.26380).
  2. ↑ Kathryn Haskins, Mary Portas, Brenda Bradley, Dale Wegmann, Kevin Lafferty: T-Lymphocyte Clone Specific for Pancreatic Islet Antigen . In: Diabetes . tape 37 , no. October 10 , 1988, pp. 1444–1448 , doi : 10.2337 / diab.37.10.1444 ( PDF ).