The NOD mouse beyond autoimmune diabetes
Article [Version publiée]
Fait partie de
Frontiers in immunology ; vol. 13.Éditeur·s
Frontiers MediaAuteur·e·s
Affiliation
Résumé·s
Autoimmune diabetes arises spontaneously in Non-Obese Diabetic (NOD) mice, and the
pathophysiology of this disease shares many similarities with human type 1 diabetes.
Since its generation in 1980, the NOD mouse, derived from the Cataract Shinogi strain,
has represented the gold standard of spontaneous disease models, allowing to
investigate autoimmune diabetes disease progression and susceptibility traits, as well
as to test a wide array of potential treatments and therapies. Beyond autoimmune
diabetes, NOD mice also exhibit polyautoimmunity, presenting with a low incidence of
autoimmune thyroiditis and Sjögren’s syndrome. Genetic manipulation of the NOD strain
has led to the generation of new mouse models facilitating the study of these and other
autoimmune pathologies. For instance, following deletion of specific genes or via insertion
of resistance alleles at genetic loci, NOD mice can become fully resistant to autoimmune
diabetes; yet the newly generated diabetes-resistant NOD strains often show a high
incidence of other autoimmune diseases. This suggests that the NOD genetic
background is highly autoimmune-prone and that genetic manipulations can shift the
autoimmune response from the pancreas to other organs. Overall, multiple NOD variant
strains have become invaluable tools for understanding the pathophysiology of and for
dissecting the genetic susceptibility of organ-specific autoimmune diseases. An
interesting commonality to all autoimmune diseases developing in variant strains of the
NOD mice is the presence of autoantibodies. This review will present the NOD mouse as a
model for studying autoimmune diseases beyond autoimmune diabetes.