The NOD Mouse as a Model of SLE

In addition to developing a high incidence of type 1 diabetes caused by a specific autoimmune response against pancreatic β cells in the islets of Langerhans, NOD mice also demonstrate spontaneous autoimmunity to other targets including the thymus, adrenal gland, salivary glands, thyroid, testis, nu...

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Bibliographic Details
Published in:Autoimmunity (Chur, Switzerland) Switzerland), 2001, Vol.34 (1), p.53-64
Main Authors: Silveira, Pablo A., Baxter, Alan G.
Format: Article
Language:English
Subjects:
Animals
BCG Vaccine - administration & dosage
Biological and medical sciences
Chromosome Mapping
Crosses, Genetic
Disease Models, Animal
General aspects
Genetic Linkage
Humans
Immunopathology
Lupus Erythematosus, Systemic - etiology
Lupus Erythematosus, Systemic - genetics
Lupus Erythematosus, Systemic - immunology
Lupus Erythematosus, Systemic - prevention & control
Medical sciences
Mice
Mice, Inbred BALB C
Mice, Inbred NOD - genetics
Mice, Inbred NOD - immunology
NOD mice
SLE
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Summary:In addition to developing a high incidence of type 1 diabetes caused by a specific autoimmune response against pancreatic β cells in the islets of Langerhans, NOD mice also demonstrate spontaneous autoimmunity to other targets including the thymus, adrenal gland, salivary glands, thyroid, testis, nuclear components and red blood cells. Moreover, treatment of pre-diabetic NOD mice with an intravenous dose of heat killed Mycobacterium bovis (M. bovis; bacillus Calmette-Guerin (BCG)) protects them from developing type 1 diabetes, but instead precipitates an autoimmune rheumatic disease similar to systemic lupus erythematosus (SLE), characterised by accelerated and increased incidence of haemolytic anaemia (HA), anti-nuclear autoantibody (ANA) production, exacerbation of sialadenitis, and the appearance of immune complex-mediated glomerulonephritis (GN). The reciprocal switching between the two phenotypes by a single environmental trigger (mycobacterial exposure) raised the possibility that genetic susceptibility for type 1 diabetes and SLE may be conferred by a single collection of genes in the NOD mouse. This review will focus on the genetic components predisposing NOD mice to SLE induced by BCG treatment and compare them to previously determined diabetes susceptibility genes in this strain and SLE susceptibility genes in the BXSB, MRL and the New Zealand mouse strains
ISSN:0891-6934
1607-842X
DOI:10.3109/08916930108994126