SCID

Strain details
Nomenclature	C.B-17/IcrHanHsd-Prkdc^scid/Ozarc
Common name	SCID
Synonyms	SCID, CB17
Strain	Mutant inbred
Coat Colour	Albino (A/A Tyrp1b/Tyrp1b Tyrc/Tyrc)
Species	Mouse
Genetic background	-
Location	Area Oz1
Weekly wean target	<10 males, <10 females

Strain descriptions

MHC haplotype: H2K^d
Complement factor: C5 normal
Arose as a spontaneous autosomal recessive mutation in C.B-Igh-1b (CB-17) congenic strain. Prkdc^scid (autosomal recessive, protein kinase, DNA activated, catalytic polypeptide).
Homozygotes have little or no immunoglobulin in serum. Lymphoid organs consist of vascular connective tissue and macrophages and are devoid of lymphocytes.
Bone marrow lacks plasma cells and lymphocytes and skin lacks dendritic Thy-1⁺ epidermal cells. Although B and T-cells, pre-B and pre-T cells are absent early B and T-cells are present.
A variable percentage (2-20%) of young adults develops low numbers of functional B and T-cells. This is not genetically determined.
Macrophage activation and antigen presentation, NK cell activity and myeloid cell differentiation is normal.
Thymic lymphomas occur in about 15% of mice.
Cystitis in female stock.
This stock strain is housed in an isolator.

In 1980 at Fox chase Canser Centre this mutation was discovered by Bosma. This mutation occurred in the C.B-17/Icr strain, IgH congenic partner of BALB/cAnIcr differing from it only by a portion of chromosome 12 that was derived from C57BL/Ka strain. In 1989, to Central Institute for Laboratory Animal Breeding, Hannover, Germany. Then to Harlan UK in 1994. Breeders refreshed with mice from Harlan UK Ltd. 2003.
SCID mice are transferred from Animal Resource Centre to Ozgene ARC in 2023.

Useful model for studying the relationship between immunity and disease, studies on engraftment of xenogenic cells and tissues, and studying human severe combined immunodeficiency.
Useful model for understanding the basis of increased lymphoid malignancies in immunodeficiencies as thymic lymphomas occurs in about 15% of mice.