List of models
Type: Mutant congenic mouse
Colour and related genotype: Albino mouse, Tyrc/Tyrc - MHC: Haplotype H2g7
Origin: INSERM Saint Vincent de Paul - (Paris, France, via CDTA, Orléans) - 2010
Breeding: Animal easy to rear, strong maternal instinct, Mating scheme: homozygous ♂ x homozygous ♀
Description of our model
The scid (Severe Combined Immunodeficiency) mutation was discovered in a colony of inbred BALB/c-Ighb (CB-17/Icr, BALB/c congenic background with Ighb-Cb allel from the C57BL/Ka strain) mice in 1980 by Dr. M.J. Bosma and his team, at the Fox Chase Cancer Center (Philadelphia, PA).
This recessive autosomal mutation impairs lymphoid differentiation. These mice are deficient in T and B cells but myelopoiesis is not affected. On a NOD background, antigen-presenting 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.
Some NOD-prkdcscid mice can become "leaky" from the spontaneous development of functional T and B lymphocytes. The presence of the prkdcscid mutation does not allow for the phonotypical expression of the type I diabetes that characterizes the NOD background (Non Obese Diabetic).
NOD SCID mice survive under SOPF conditions for 8 to 9 months (before the development of thymic lymphoma).
Our added value
The « JANVIER LABS Genetic Policy », a specific programme, the homogeneity of the genetic background, identic to the wild types used as controls.
Animals with the SOPF standards.
A gentling policy for docile and easy-to-handle animals.
Optimal stability conditions of our models during shipments, thanks to our dedicated and internal transport service.
A scientific support with a team of Veterinarians and PhD.
Download the corresponding health monitoring reports