SCID mice

SCID mice

SCID mice

Strain details
NomenclatureC.B-17/IcrHanHsd-Prkdcscid/Ozarc
Common nameSCID
SynonymsCB17, C.B-17 scid
StrainMutant inbred
Coat ColourAlbino (A/A Tyrp1b/Tyrp1b Tyrc/Tyrc)
SpeciesMouse
Genetic backgroundCongenic
LocationArea Oz1
Weekly wean target<10 males, <10 females

Strain description

  • MHC haplotype: H2Kd
  • Complement factor: C5 normal
  • Arose as a spontaneous autosomal recessive mutation in C.B-Igh-1b (CB-17) congenic strain. Prkdcscid (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.

Past ARC and transfer reports:

Current Ozgene ARC reports (from 01-Jun-2023)

  • Mouse images are representative only. Actual phenotypes may vary based on genotype, sex, age, husbandry, health status, and other factors.
  • Li Z, et al. Rev Assoc Med Bras. 2021 Nov;67(11):1735-1738. PMID: 34730675 doi: 10.1590/1806-9282.20210715. Progress and application on severe combined immunodeficiency mouse model for rheumatoid arthritis: a literature review
  • Yoshida M, et al. Cancer Res. 1997 Feb 15;57(4):678-85. PMID: 9044845. Development of a Severe Combined Immunodeficiency (SCID) mouse model consisting of highly disseminated human B-cell leukemia/lymphoma.
  • Lee JY, et al. Biol Sci Life. 2015 Jun;21(2):51-59 doi: 10.15616/BSL.2015.21.2.51. Humanized (SCID) Mice as a Model to Study Human Leukemia.

SCID mice: Crucial model for immunodeficiency and human disease research

SCID (Severe Combined Immunodeficiency) mice are a valuable tool in biomedical research due to their profound immunodeficiency, making them ideal for various studies, including human disease modelling and transplantation research. SCID mice carry a mutation in the Prkdc gene, which is essential for the repair of DNA double-strand breaks.

The Prkdc mutation impairs the development and maturation of lymphocytes, leading to a lack of functional T and B cells. This immunodeficiency allows for the engraftment of human tissues and cells, as the mice lack an adaptive immune response that would typically reject these foreign cells.

The SCID mutation causes a defect in the V(D)J recombination process necessary for generating diverse antigen receptors on T and B cells. This defect results in severe immunodeficiency, characterized by a complete absence of functional lymphocytes. However, unlike other immunodeficient strains, SCID mice retain some residual natural killer (NK) cell activity.

Application and Research

  • Xenograft and patient-derived xenograft (PDX) models: SCID mice are frequently used for engrafting human tumours, providing a robust model for studying tumour biology, progression, and response to therapeutics. These models closely mimic human cancer and are essential for translational cancer research.
  • Tumour microenvironment studies: These mice enable the examination of how the tumour microenvironment affects cancer progression and treatment response. The immunodeficient status of SCID mice allows human tumour cells to interact with surrounding tissues without immune rejection.
  • Immunotherapy development: SCID mice are utilized to test immunotherapies, especially when combined with human immune cell transplantation to create a humanized immune system. This setup permits researchers to observe human immune cell responses to cancer therapies in a controlled environment.
  • Immune system research: SCID mice serve as a model to study immune system deficiencies and the development of immune cells. By reconstituting SCID mice with human hematopoietic stem cells, researchers can investigate human immune cell development and function.
  • Transplantation research: The lack of an adaptive immune response in SCID mice makes them ideal recipients for human tissue and organ transplants, facilitating studies on graft acceptance and rejection mechanisms.
  • Gene therapy studies: SCID mice are used to evaluate gene therapy approaches aimed at correcting immune deficiencies. These studies provide critical insights into the potential therapeutic applications of gene editing technologies.
  • Genetic mutation effects: Researchers utilize SCID mice to understand the impact of specific genetic mutations on immune function and overall health.
  • Pharmacological testing: SCID mice are employed to test the efficacy and safety of new drugs, particularly those targeting the immune system or requiring human cell models for accurate evaluation.
  • Toxicology studies: The immunodeficient nature of SCID mice makes them suitable for toxicology studies, where researchers can assess the adverse effects of new compounds in the absence of a fully functional immune system.