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. Prkdcscid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. In general, Prkdcscid leakiness is low on the NOD/ShiLtSz genetic background.
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Allele Type | Gene Symbol | Gene Name |
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Spontaneous | Prkdc | protein kinase, DNA activated, catalytic polypeptide |
Allele Type | Gene Symbol | Gene Name |
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Spontaneous | Hc | hemolytic complement |
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 the C3H/HeJ background, and even lower on the NOD/ShiLtSz background. NOD/ShiLtSz-Prkdcscid mice are both insulitis- and diabetes-free throughout life and serve as a diabetes-free control for comparison to NOD/ShiLtJ mice (Stock No. 001976). Thymic lymphomas occur with high frequency, however, and life span typically is limited to only 8.5 months under specific pathogen-free conditions. In addition to being an excellent host for xenografts, NOD.CB17-Prkdcscid/J mice may be useful for delineation of the role of T cell subsets in autoimmune diabetes and also as a source for insulitis-free islets.
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. The Prkdcscid mutation was backcrossed onto the NOD/ShiLtSz background as follows: an NOD/ShiLtSz female was bred to a C.B-17-Prkdcscid male; male Prkdcscid/+ offspring of the F1/N1 and subsequent generations were mated to NOD/ShiLt females for a total of 10 crosses to NOD/ShiLtSz; at generation N10, Prkdcscid was made homozygous by brother-sister inbreeding.
Allele Name | severe combined immunodeficiency |
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Allele Type | Spontaneous |
Allele Synonym(s) | SCID |
Gene Symbol and Name | Prkdc, protein kinase, DNA activated, catalytic polypeptide |
Gene Synonym(s) | |
Site of Expression | T and B lymphocytes. |
Strain of Origin | C.BKa-Ighb/Icr |
Chromosome | 16 |
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*). |
Allele Name | deficient |
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Allele Type | Spontaneous |
Allele Synonym(s) | C5-; C5-d; C5-def; C5-deficient; HcHfib2; hco |
Gene Symbol and Name | Hc, hemolytic complement |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 2 |
General Note | This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211) |
Molecular Note | A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, A/J, AKR/J, DBA/2J, I/LnJ, KK/HlJ, MOLF/EiJ, NZB/B1NJ, RF/J, ST/bJ SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5. |
When using the NOD scid mouse strain in a publication, please cite the originating article(s) and include JAX stock #001303 in your Materials and Methods section.
Service/Product | Description | Price |
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Homozygous for Prkdc<scid>, 1 pair minimum |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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