Commonly referred to as BALB/c scid, these animals carry the severe combined immune deficiency mutation (scid) on the BALB/c background. This strain is very similar to the original BALB/c-Ighb scid (C.B-17 scid) strain maintained at the Institute for Cancer Research in Philadelphia, PA. Compared with our most popular scid mutant strain (NOD-scid, Stock No. 001303), the BALB/c scid does not carry the C5 complement deficient mutation, thus enabling Complement-Dependent Cytotoxicity (CDC), a major pharmacological effect of therapeutic antibodies. This is the strain of choice for efficacy testing of therapeutic antibodies in the context of transplantable tumor host.Read More +
Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain dependent, increases with age, and is higher in mice housed under non-SPF conditions. In general, scid leakiness is high on the C57BL/6J and BALB/cBy genetic backgrounds, low on C3H/HeJ background, and even lower on the NOD/ShiLtSz background. Note: BALB/cBy mice are Igh-1a while the original C.B-17 mice are Igh-1b.
View Flow Cytometry Characterization Data for Immunodeficient JAX Strains
Prkdcscid occurred spontaneously in a colony of BALB/c-Ighb (C.B-17) mice maintained at the Institute for Cancer Research in Philadelphia, PA. It was transferred to BALB/cByJSmn by Charles Sidman (Roths et al. and personal communication).
|Allele Name||severe combined immunodeficiency|
|Gene Symbol and Name||Prkdc, protein kinase, DNA activated, catalytic polypeptide|
|Site of Expression||T and B lymphocytes.|
|Strain of Origin||C.BKa-Ighb/Icr|
|Molecular Note||A T-to-A transversion point mutation at a position corresponding to codon 4046 (codon 4095 in transcript ENSMUST00000023352.8) created a premature stop codon (p.Y4046*).|
When using the CBySmn.Cg-Prkdcscid/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #001803 in your Materials and Methods section.