CB17-SCID Immundeficient Mouse

The scid (Severe Combined Immunodeficiency) mutation was discovered by Dr. M. J. Bosma and his team in the 1980s at the Fox Chase Cancer Center (Philadelphia, USA).

The mutation appeared in a colony of inbred BALB/c-Ighb (CB-17/Icr, BALB/c congenic background with Ighb-Cb allel from the C57BL/Ka strain). This recessive autosomal muta􀆟 on is characterized by an absence of functional T cells and B cells, a lymphopenia, a hypogammaglobulinemia and a normal hematopoietic environment.
The activity of the antigen-presenting cells (APC), myeloid cells and the functions of Natural Killer cells (NK) depend on the genetic background the mutation is transferred to.

Most homozygotes do not have any detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA.

Some SCID mice can spontaneously develop a partial immune reactivity: the “leaky” mouse.

This strain has a shorter lifetime in a conventional environment. However, under SOPF conditions, the CB17-SCID mouse survives for up to a year.

Main application and research fields