NOD-SCID immunodeficient mouse
Immunodeficient mouse for immunology and oncology research
Souris congénique mutante
INSERM Saint Vincent de Paul (Paris, France, via CDTA, Orléans) - 2010
Colour and related genotype:
Souris albinos, A/A, Tyrc/Tyrc - MHC : Haplotype H2g7
Description of our model and application areas
The scid (Severe Combined Immunodefi ciency) muta on was discovered by Dr. M.J. Bosma and his team in the 1980s at the Fox Chase Cancer Center (Philadelphia, PA). It appeared in a colony of inbred BALB/c-Ighb (CB-17/Icr mice, BALB/c congenic background with Ighb-Cb allel from the C57BL/Ka strain). This recessive autosomal muta on is characterized by an absence of B cells and functional T cells, a lymphopenia, a hypogammaglobulinemia and a normal hematopoietic environment. On a NOD background, antigenpresenting cells’ (APC), myeloid cells’ and the NK cell functions are impaired.
Most homozygotes do not have any detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. However, some NOD-prkdcscid mice can spontaneously develop a partial immune reactivity: the “leaky” mouse. The presence of the prkdcscid mutation does not allow for the phenotypical expression of the type I diabetes that characterizes the NOD background (Non Obese Diabetic).
This model can survive up to 8 to 9 months due to the spontaneous development of thymic lymphoma.
Main application and research fields
Flow cytometry analysis, spleen
This model has been entirely characterized. The immunological and hematological parameters were characterized by Center of Immunophenomics (Ciphe, Marseille, France).
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