CB17-SCID Immundeficient Mouse
Mutant congenic mouse
Institut Pasteur (Lille, France) – 2009
Colour and related genotype:
Albino mouse, Tyrp1b/Tyrp1b, Tyrc/Tyrc - MHC : Haplotype H2d
Description of our model and application areas
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
The growth curve represents an average which reflects the weight variation of the strain measured between 21 and 84 days for males and females.
of 10-week old CB17 Scid mice
Flow cytometry analysis, spleen
All lymphoid organs of our models were analysed
This model has been entirely characterized. The immunological and hematological parameters were characterized by Center of Immunophenomics (Ciphe, Marseille, France).
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