NOD-SCID immunodeficient mouse

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-prkdc^scid mice can spontaneously develop a partial immune reactivity: the “leaky” mouse. The presence of the prkdc^scid 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