JAX Mouse Strain Datasheet - 001303

NOD.CB17-Prkdc^scid/J

Stock No:: 001303 |; NOD scid

Spontaneous Mutation

Readily Available

Overview

Also Known As: NOD scid, NOD SCID

Mice homozygous for the severe combined immune deficiency spontaneous mutation Prkdc^scid, commonly referred to as scid, are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Prkdc^scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. In general, Prkdc^scid leakiness is low on the NOD/ShiLtSz genetic background.

Genetic overview

Genetic Background	Generation
NOD/ShiLtSz	N10F58pF62 (14-AUG-14)

Hc⁰

Allele Type	Gene Symbol	Gene Name
Spontaneous	Hc	hemolytic complement

Prkdc^scid

Allele Type	Gene Symbol	Gene Name
Spontaneous	Prkdc	protein kinase, DNA activated, catalytic polypeptide

View Genetics

Research Applications

Cancer Research
Diabetes and Obesity Research
Research Tools
Immunology, Inflammation and Autoimmunity Research
Internal/Organ Research
Virology Research

View All Research Applications

Base Price

Starting at:

$101.70 Domestic price for male 3-week

View Price List

Details

Detailed Description

Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdc^scid, 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-Prkdc^scid 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-Prkdc^scid/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

Development

Prkdc^scid occurred spontaneously in a colony of BALB/c-Igh^b (C.B-17) mice maintained at the Institute for Cancer Research in Philadelphia, PA. The Prkdc^scid mutation was backcrossed onto the NOD/ShiLtSz background as follows: an NOD/ShiLtSz female was bred to a C.B-17-Prkdc^scid male; male Prkdc^scid/+ 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, Prkdc^scid was made homozygous by brother-sister inbreeding.

Control Suggestions

Selection of control mice depends upon the nature of the research.
001976 NOD/ShiLtJ

Additional Information

Considerations for Choosing Controls

Selected References

Blunt T; Finnie NJ; Taccioli GE; Smith GC; Demengeot J; Gottlieb TM; Mizuta R; Varghese AJ; Alt FW; Jeggo PA; Jackson SP. 1995. Defective DNA-dependent protein kinase activity is linked to V(D)J recombination and DNA repair defects associated with the murine scid mutation. Cell 80(5):813-23. PubMed: 7889575 MGI: J:30365
Blunt T; Gell D; Fox M; Taccioli GE; Lehmann AR; Jackson SP; Jeggo PA. 1996. Identification of a nonsense mutation in the carboxyl-terminal region of DNA-dependent protein kinase catalytic subunit in the scid mouse. Proc Natl Acad Sci U S A 93(19):10285-90. PubMed: 8816792 MGI: J:35393
Bosma M; Schuler W; Bosma G. 1988. The scid mouse mutant. Curr Top Microbiol Immunol 137:197-202. PubMed: 3416632 MGI: J:9341
Christianson SW; Shultz LD; Leiter EH. 1993. Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. Diabetes 42(1):44-55. PubMed: 8093606 MGI: J:34990
Hudson WA; Li Q; Le C; Kersey JH. 1998. Xenotransplantation of human lymphoid malignancies is optimized in mice with multiple immunologic defects. Leukemia 12(12):2029-33. PubMed: 9844934 MGI: J:153650
Many MC; Drexhage HA; Denef JF. 1993. High frequency of thymic ectopy in thyroids from autoimmune prone nonobese diabetic female mice. Lab Invest 69(3):364-7. PubMed: 8377477 MGI: J:14747
Nonoyama S; Smith FO; Bernstein ID; Ochs HD. 1993. Strain-dependent leakiness of mice with severe combined immune deficiency. J Immunol 150(9):3817-24. PubMed: 8473734 MGI: J:4610
Prochazka M; Gaskins HR; Shultz LD; Leiter EH. 1992. The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency. Proc Natl Acad Sci U S A 89(8):3290-4. PubMed: 1373493 MGI: J:513
Serreze DV; Leiter EH; Hanson MS; Christianson SW; Shultz LD; Hesselton RM; Greiner DL. 1995. Emv30null NOD-scid mice. An improved host for adoptive transfer of autoimmune diabetes and growth of human lymphohematopoietic cells. Diabetes 44(12):1392-8. PubMed: 7589844 MGI: J:29951
Shultz LD; Schweitzer PA; Christianson SW; Gott B; Schweitzer IB; Tennent B; McKenna S; Mobraaten L; Rajan TV; Greiner DL; Leiter EH. 1995. Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice. J Immunol 154(1):180-91. PubMed: 7995938 MGI: J:22026

View All References

Genetics

Hc⁰

Allele Symbol: Hc⁰

Allele Name	deficient
Allele Type	Spontaneous
Allele Synonym(s)	C5-; C5-d; C5-def; C5-deficient; Hc^Hfib2; hc^o
Gene Symbol and Name	Hc, hemolytic complement
Gene Synonym(s)	C5; C5; C5D; C5a; C5b; CPAMD4; ECLZB; He; He; Hfib2; Hfib2; hepatic fibrogenesis 2
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, NZB/B1NJ, 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.

Prkdc^scid

Allele Symbol: Prkdc^scid

Allele Name	severe combined immunodeficiency
Allele Type	Spontaneous
Allele Synonym(s)	SCID; scid
Gene Symbol and Name	Prkdc, protein kinase, DNA activated, catalytic polypeptide
Gene Synonym(s)	AI326420; AU019811; DNA-PK; DNA-PKcs; DNAPDcs; DNAPK; DNPK1; DOXNPH; HYRC; HYRC1; IMD26; XRCC7; doxorubicin nephropathy; dxnph; dxnph; expressed sequence AI326420; expressed sequence AU019811; p350; scid; severe combined immunodeficiency; slip
Site of Expression	T and B lymphocytes.
Strain of Origin	C.B-17
Chromosome	16
Molecular Note	A T-to-A transversion point mutation at a position corresponding to codon 4095 created a premature stop codon.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Cancer Research
- Increased Tumor Incidence
  - Lymphomas
  - Lymphomas: thymic
Diabetes and Obesity Research
- Islet Transplantation Studies
- Type 1 Diabetes (IDDM) Analysis Strains
  - NOD Congenics with Mutations Affecting Immunocompetence
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - B and T cell deficiency

Genotype: Hc⁰ related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - specific complement deficiency
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - specific complement deficiency, C5 complement

Genotype: Prkdc^scid related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - B and T cell deficiency
Internal/Organ Research
- Lymphoid Tissue Defects
  - B and T cell deficiency
Research Tools
- Cancer Research
  - B and T cell deficiency, xenograft/transplant host
- Toxicology Research
  - xenograft/transplant host
Virology Research
- B and T Cell Deficiency
  - AIDS research tool

Mammalian Phenotype Terms by Genotype

Genotype: Prkdc^scid/Prkdc^scid
NOD.CB17-Prkdc^scid/J

homeostasis/metabolism phenotype

increased circulating glucose level
- following intraperitoneal injection of human peripheral blood mononuclear cells, 11 of 12 streptozotocin-treated mice engrafted with human islet cells exhibit increased glucose serum levels although not as high as pre-transplantation
- following treatment with streptozotocin, mice exhibit increased glucose serum levels that can be restored to euglycemic levels by engraftment of human islet cells

immune system phenotype

abnormal response to transplant
- however, this rejection is not due to graft versus host disease
- while human islet engrafts in streptozotocin-treated mice appear normal after 4 weeks, subsequent injection of human peripheral blood mononuclear cells results in destructive infiltrate into the human islet graft site, inflammation, loss of engrafted islet beta cells, fibrosis, and necrosis after 3 weekst beta cells, fibrosis, and necrosis after 3 weeks

Genotype: Prkdc^scid/Prkdc^scid
NOD.CB17-Prkdc^scid

mortality/aging

premature death
- average lifespan in SPF housing is 257 days for females and 269 days for males
- median life span is 37 weeks; death is a result of thymic lymphomas
- the major cause of death is thymic lymphoma

immune system phenotype

abnormal lymph node morphology
- lymph nodes are hypocellular
- lymph nodes lack follicles and consist mostly of stromal cells

abnormal response to transplant
- following injection of human T lymphoblastoid cells, 80% of nucleated spleen cells are of human origin by 4 weeks post injection
- human CD45+ cells comprise 5.2% of cells in the spleen, 6.2% in bone marrow, 0.4% in thymus at 10 weeks post-engraftment
- mice support CD34+ human stem cell engraftment, although not as well as mice homozygous for Il2rg^tm1Wjl and Prkdc^scid
- peripheral blood has a five fold increase of human cells by 4 weeks post injection

abnormal spleen white pulp morphology
- splenic follicles are hypoplastic
- splenic follicles exhibit a marked loss of lymphoid cells, however, red pulp is normal

abnormal thymus corticomedullary boundary morphology
- the cortico-medullary junction is not demarcated in tissues from a 10 week old female

abnormal thymus lobule morphology
- thymic lobes are small and may contain cysts

decreased B cell number
- B220+ splenic B cells are decreased (36.0% vs. 10.4%) in comparison to NOD control as measured by flow cytometry

decreased CD4-positive, alpha beta T cell number
- spleens are deficient in mature T cells

decreased CD8-positive, alpha-beta T cell number
- spleens are deficient in mature T cells

decreased NK cell number
- no NK1.1+ splenic NK cells were detected by flow cytometry, however some NK cell activity is detected

decreased T cell number
- significant numbers of CD3+ splenic T cells are absent in comparison to control (44.9% vs. 0.2%)

decreased immunoglobulin level
- only 1/11 homozygotes can produce greater than 1 ug/ml serum Ig at up to 100 days of age
- only 2/30 homozygotes can produce greater than 1 ug/ml serum Ig between 100-200 days of age

decreased level of surface class I molecules

decreased lymphocyte cell number
- percentages of circulating lymphocytes are significantly decreased in comparison to control, however, percentages of monocytes, neutrophils and eosinophils are increased and total peripheral leukocyte counts are similar
- thymus, spleen and lymph nodes are depleted of lymphoid cells

decreased mature B cell number
- spleens are deficient in B220+ IgK+ B cells

decreased pre-B cell number
- B220+ bone marrow pre-B cells are decreased in number (19.0% vs. 10.2%)
- there is a significant absence of splenic B cells bearing the Ig kappa light chain (30.7% vs. 2.8%)

impaired complement classical pathway
- complement activity is not detected in either homozygous or control sera using a 51Cr-release assay

impaired natural killer cell mediated cytotoxicity
- Background Sensitivity - NK cell activity in homozygous spleen cell suspensions is markedly decreased in comparison to homozygotes on the CB17 background

increased granulocyte number
- Gr1+ splenic and bone marrow granulocytes are increased in comparison to control

increased length of allograft survival
- homozygotes (5-6 weeks of age) do not reject orthotopic tail skin allografts throughout a 3 month observation period

increased macrophage cell number
- F4/80+ splenic macrophages are increased in comparison to control

spleen hypoplasia
- spleen cellularity is decreased four fold in comparison to NOD control
- splenic follicles are hypoplastic

thymus cysts
- may be present

hematopoietic system phenotype

abnormal spleen white pulp morphology
- splenic follicles are hypoplastic
- splenic follicles exhibit a marked loss of lymphoid cells, however, red pulp is normal

abnormal thymus corticomedullary boundary morphology
- the cortico-medullary junction is not demarcated in tissues from a 10 week old female

abnormal thymus lobule morphology
- thymic lobes are small and may contain cysts

decreased B cell number
- B220+ splenic B cells are decreased (36.0% vs. 10.4%) in comparison to NOD control as measured by flow cytometry

decreased CD4-positive, alpha beta T cell number
- spleens are deficient in mature T cells

decreased CD8-positive, alpha-beta T cell number
- spleens are deficient in mature T cells

decreased NK cell number
- no NK1.1+ splenic NK cells were detected by flow cytometry, however some NK cell activity is detected

decreased T cell number
- significant numbers of CD3+ splenic T cells are absent in comparison to control (44.9% vs. 0.2%)

decreased bone marrow cell number
- homozygotes have a 40% reduction in nucleated bone marrow cells compared to NOD control

decreased erythrocyte cell number
- homozygotes have significantly reduced erythrocyte counts in contrast to NOD control

decreased immunoglobulin level
- only 1/11 homozygotes can produce greater than 1 ug/ml serum Ig at up to 100 days of age
- only 2/30 homozygotes can produce greater than 1 ug/ml serum Ig between 100-200 days of age

decreased lymphocyte cell number
- percentages of circulating lymphocytes are significantly decreased in comparison to control, however, percentages of monocytes, neutrophils and eosinophils are increased and total peripheral leukocyte counts are similar
- thymus, spleen and lymph nodes are depleted of lymphoid cells

decreased mature B cell number
- spleens are deficient in B220+ IgK+ B cells

decreased pre-B cell number
- B220+ bone marrow pre-B cells are decreased in number (19.0% vs. 10.2%)
- there is a significant absence of splenic B cells bearing the Ig kappa light chain (30.7% vs. 2.8%)

impaired natural killer cell mediated cytotoxicity
- Background Sensitivity - NK cell activity in homozygous spleen cell suspensions is markedly decreased in comparison to homozygotes on the CB17 background

increased granulocyte number
- Gr1+ splenic and bone marrow granulocytes are increased in comparison to control

increased macrophage cell number
- F4/80+ splenic macrophages are increased in comparison to control

increased mean corpuscular volume
- Background Sensitivity - erythrocyte mean cell volume is elevated in both homozygotes and NOD controls in contrast to homozygotes on the CB17 background

spleen hypoplasia
- spleen cellularity is decreased four fold in comparison to NOD control
- splenic follicles are hypoplastic

thymus cysts
- may be present

homeostasis/metabolism phenotype

homeostasis/metabolism phenotype
- mice do not develop insulitis in contrast to NOD controls
- weekly monitoring of urinary glucose demonstrates that mice do not develop diabetes

neoplasm

increased T cell derived lymphoma incidence
- lymphomas metastasize to multiple sites and are the major cause of death

cellular phenotype

increased cellular sensitivity to X-ray irradiation
- mice do not survive doses above 400 cGy
- some irradiated mice exhibit thymic lymphomas or mitotic figures following irradiation

endocrine/exocrine gland phenotype

abnormal thymus corticomedullary boundary morphology
- the cortico-medullary junction is not demarcated in tissues from a 10 week old female

abnormal thymus lobule morphology
- thymic lobes are small and may contain cysts

increased T cell derived lymphoma incidence
- lymphomas metastasize to multiple sites and are the major cause of death

thymus cysts
- may be present

Phenotype Information

Body Weight Information - JAX^® Mice Strain NOD.CB17-Prkdc^scid/J (001303)

JAX^® Physiological Data Summary [pdf]

References

Blunt T; Finnie NJ; Taccioli GE; Smith GC; Demengeot J; Gottlieb TM; Mizuta R; Varghese AJ; Alt FW; Jeggo PA; Jackson SP. 1995. Defective DNA-dependent protein kinase activity is linked to V(D)J recombination and DNA repair defects associated with the murine scid mutation. Cell 80(5):813-23. PubMed: 7889575 MGI: J:30365
Blunt T; Gell D; Fox M; Taccioli GE; Lehmann AR; Jackson SP; Jeggo PA. 1996. Identification of a nonsense mutation in the carboxyl-terminal region of DNA-dependent protein kinase catalytic subunit in the scid mouse. Proc Natl Acad Sci U S A 93(19):10285-90. PubMed: 8816792 MGI: J:35393
Bosma M; Schuler W; Bosma G. 1988. The scid mouse mutant. Curr Top Microbiol Immunol 137:197-202. PubMed: 3416632 MGI: J:9341
Christianson SW; Shultz LD; Leiter EH. 1993. Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4+ and CD8+ T-cells from diabetic versus prediabetic NOD.NON-Thy-1a donors. Diabetes 42(1):44-55. PubMed: 8093606 MGI: J:34990
Hudson WA; Li Q; Le C; Kersey JH. 1998. Xenotransplantation of human lymphoid malignancies is optimized in mice with multiple immunologic defects. Leukemia 12(12):2029-33. PubMed: 9844934 MGI: J:153650
Many MC; Drexhage HA; Denef JF. 1993. High frequency of thymic ectopy in thyroids from autoimmune prone nonobese diabetic female mice. Lab Invest 69(3):364-7. PubMed: 8377477 MGI: J:14747
Nonoyama S; Smith FO; Bernstein ID; Ochs HD. 1993. Strain-dependent leakiness of mice with severe combined immune deficiency. J Immunol 150(9):3817-24. PubMed: 8473734 MGI: J:4610
Prochazka M; Gaskins HR; Shultz LD; Leiter EH. 1992. The nonobese diabetic scid mouse: model for spontaneous thymomagenesis associated with immunodeficiency. Proc Natl Acad Sci U S A 89(8):3290-4. PubMed: 1373493 MGI: J:513
Serreze DV; Leiter EH; Hanson MS; Christianson SW; Shultz LD; Hesselton RM; Greiner DL. 1995. Emv30null NOD-scid mice. An improved host for adoptive transfer of autoimmune diabetes and growth of human lymphohematopoietic cells. Diabetes 44(12):1392-8. PubMed: 7589844 MGI: J:29951
Shultz LD; Schweitzer PA; Christianson SW; Gott B; Schweitzer IB; Tennent B; McKenna S; Mobraaten L; Rajan TV; Greiner DL; Leiter EH. 1995. Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice. J Immunol 154(1):180-91. PubMed: 7995938 MGI: J:22026

Additional References

Alexander AM; Crawford M; Bertera S; Rudert WA; Takikawa O; Robbins PD; Trucco M. 2002. Indoleamine 2,3-dioxygenase expression in transplanted NOD Islets prolongs graft survival after adoptive transfer of diabetogenic splenocytes. Diabetes 51(2):356-65. PubMed: 11812742 MGI: J:74301
Beamer WG; Shultz KL; Tennent BJ; Shultz LD. 1993. Granulosa cell tumorigenesis in genetically hypogonadal-immunodeficient mice grafted with ovaries from tumor-susceptible donors. Cancer Res 53(16):3741-6. PubMed: 8339285 MGI: J:14443
Chen AM; Zhou Y; Swenson K; Sachs DH; Sykes M; Yang YG. 2000. Porcine stem cell engraftment and seeding of murine thymus with class II+ cells in mice expressing porcine cytokines: toward tolerance induction across discordant xenogeneic barriers. Transplantation 69(12):2484-90. PubMed: 10910267 MGI: J:93486
Chiu PP; Ivakine E; Mortin-Toth S; Danska JS. 2002. Susceptibility to lymphoid neoplasia in immunodeficient strains of nonobese diabetic mice. Cancer Res 62(20):5828-34. PubMed: 12384545 MGI: J:79669
Custer RP; Bosma GC; Bosma MJ. 1985. Severe combined immunodeficiency (SCID) in the mouse. Pathology, reconstitution, neoplasms. Am J Pathol 120(3):464-77. PubMed: 2412448 MGI: J:30980
Dorshkind K; Keller GM; Phillips RA; Miller RG; Bosma GC; O'Toole M; Bosma MJ. 1984. Functional status of cells from lymphoid and myeloid tissues in mice with severe combined immunodeficiency disease. J Immunol 132(4):1804-8. PubMed: 6607948 MGI: J:7343
Glimm H; Eisterer W; Lee K; Cashman J; Holyoake TL; Nicolini F; Shultz LD; von Kalle C; Eaves CJ. 2001. Previously undetected human hematopoietic cell populations with short-term repopulating activity selectively engraft NOD/SCID-beta2 microglobulin-null mice. J Clin Invest 107(2):199-206. PubMed: 11160136 MGI: J:66974
Grattan M; Mi QS; Meagher C; Delovitch TL. 2002. Congenic mapping of the diabetogenic locus Idd4 to a 5.2-cM region of chromosome 11 in NOD mice: identification of two potential candidate subloci. Diabetes 51(1):215-23. PubMed: 11756344 MGI: J:73763
Greeley SA; Katsumata M; Yu L; Eisenbarth GS; Moore DJ; Goodarzi H; Barker CF; Naji A; Noorchashm H. 2002. Elimination of maternally transmitted autoantibodies prevents diabetes in nonobese diabetic mice. Nat Med 8(4):399-402. PubMed: 11927947 MGI: J:75803
Kanagawa O; Militech A; Vaupel BA. 2002. Regulation of diabetes development by regulatory T cells in pancreatic islet antigen-specific TCR transgenic nonobese diabetic mice. J Immunol 168(12):6159-64. PubMed: 12055228 MGI: J:89793
Kanagawa O; Shimizu J; Vaupel BA. 2000. Thymic and postthymic regulation of diabetogenic CD8 T cell development in TCR transgenic nonobese diabetic (NOD) mice. J Immunol 164(10):5466-73. PubMed: 10799914 MGI: J:62643
Karanu FN; Murdoch B; Miyabayashi T; Ohno M; Koremoto M; Gallacher L; Wu D; Itoh A; Sakano S; Bhatia M. 2001. Human homologues of Delta-1 and Delta-4 function as mitogenic regulators of primitive human hematopoietic cells. Blood 97(7):1960-7. PubMed: 11264159 MGI: J:68395
Liao C; Wang XY; Wei HQ; Li SQ; Merghoub T; Pandolfi PP; Wolgemuth DJ. 2001. Altered myelopoiesis and the development of acute myeloid leukemia in transgenic mice overexpressing cyclin A1. Proc Natl Acad Sci U S A 98(12):6853-8. PubMed: 11381140 MGI: J:69909
Maykel J; Liu JH; Li H; Shultz LD; Greiner DL; Houghton J. 2014. NOD-scidIl2rg (tm1Wjl) and NOD-Rag1 (null) Il2rg (tm1Wjl) : a model for stromal cell-tumor cell interaction for human colon cancer. Dig Dis Sci 59(6):1169-79. PubMed: 24798995 MGI: J:227975
Pauza ME; Dobbs CM; He J; Patterson T; Wagner S; Anobile BS; Bradley BJ; Lo D; Haskins K. 2004. T-cell receptor transgenic response to an endogenous polymorphic autoantigen determines susceptibility to diabetes. Diabetes 53(4):978-88. PubMed: 15047613 MGI: J:89082
Sanchez-Fueyo A; Tian J; Picarella D; Domenig C; Zheng XX; Sabatos CA; Manlongat N; Bender O; Kamradt T; Kuchroo VK; Gutierrez-Ramos JC; Coyle AJ; Strom TB. 2003. Tim-3 inhibits T helper type 1-mediated auto- and alloimmune responses and promotes immunological tolerance. Nat Immunol 4(11):1093-101. PubMed: 14556005 MGI: J:86260
Savinov AY; Tcherepanov A; Green EA; Flavell RA; Chervonsky AV. 2003. Contribution of Fas to diabetes development. Proc Natl Acad Sci U S A 100(2):628-32. PubMed: 12525697 MGI: J:81416
Schmidt RE; Dorsey DA; Beaudet LN; Frederick KE; Parvin CA; Plurad SB; Levisetti MG. 2003. Non-obese diabetic mice rapidly develop dramatic sympathetic neuritic dystrophy: a new experimental model of diabetic autonomic neuropathy. Am J Pathol 163(5):2077-91. PubMed: 14578206 MGI: J:86318
Sekiguchi J; Ferguson DO; Chen HT; Yang EM; Earle J; Frank K; Whitlow S; Gu Y; Xu Y; Nussenzweig A; Alt FW. 2001. Genetic interactions between ATM and the nonhomologous end-joining factors in genomic stability and development. Proc Natl Acad Sci U S A 98(6):3243-8. PubMed: 11248063 MGI: J:68074
Trembleau S; Gregori S; Penna G; Gorny I; Adorini L. 2001. Il-12 administration reveals diabetogenic t cells in genetically resistant i-ealpha-transgenic nonobese diabetic mice: resistance to autoimmune diabetes is associated with binding of ealpha-derived peptides to the i-a(g7) molecule. J Immunol 167(7):4104-14. PubMed: 11564833 MGI: J:71651

Additional - Hc⁰ related

Actor JK; Breij E; Wetsel RA; Hoffmann H; Hunter RL Jr; Jagannath C. 2001. A role for complement C5 in organism containment and granulomatous response during murine tuberculosis. Scand J Immunol 53(5):464-74. PubMed: 11309154 MGI: J:103981
Addis-Lieser E; Kohl J; Chiaramonte MG. 2005. Opposing regulatory roles of complement factor 5 in the development of bleomycin-induced pulmonary fibrosis. J Immunol 175(3):1894-902. PubMed: 16034133 MGI: J:107269
Anderson AL; Sporici R; Lambris J; Larosa D; Levinson AI. 2006. Pathogenesis of B-cell superantigen-induced immune complex-mediated inflammation. Infect Immun 74(2):1196-203. PubMed: 16428769 MGI: J:104987
Barthlott T; Stockinger B. 2001. Lineage fate alteration of thymocytes developing in an MHC environment containing MHC/peptide ligands with antagonist properties. Eur J Immunol 31(12):3595-601. PubMed: 11745379 MGI: J:151748
Baudino L; Sardini A; Ruseva MM; Fossati-Jimack L; Cook HT; Scott D; Simpson E; Botto M. 2014. C3 opsonization regulates endocytic handling of apoptotic cells resulting in enhanced T-cell responses to cargo-derived antigens. Proc Natl Acad Sci U S A 111(4):1503-8. PubMed: 24474777 MGI: J:206648
Bauer K; Yu X; Wernhoff P; Koczan D; Thiesen HJ; Ibrahim SM. 2004. Identification of new quantitative trait loci in mice with collagen-induced arthritis. Arthritis Rheum 50(11):3721-8. PubMed: 15529344 MGI: J:94347
Binstadt BA; Hebert JL; Ortiz-Lopez A; Bronson R; Benoist C; Mathis D. 2009. The same systemic autoimmune disease provokes arthritis and endocarditis via distinct mechanisms. Proc Natl Acad Sci U S A 106(39):16758-63. PubMed: 19805369 MGI: J:153217
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Bora NS; Kaliappan S; Jha P; Xu Q; Sohn JH; Dhaulakhandi DB; Kaplan HJ; Bora PS. 2006. Complement activation via alternative pathway is critical in the development of laser-induced choroidal neovascularization: role of factor B and factor H. J Immunol 177(3):1872-8. PubMed: 16849499 MGI: J:138026
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Also Known As: NOD scid, NOD SCID

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Hc0

Allele Symbol: Hc0

Prkdcscid

Allele Symbol: Prkdcscid

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Genotype: Hc0 related

Genotype: Prkdcscid related

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Genotype: Prkdcscid/PrkdcscidNOD.CB17-Prkdcscid/J

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Prkdcscid/PrkdcscidNOD.CB17-Prkdcscid

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Hc⁰

Allele Symbol: Hc⁰

Prkdc^scid

Allele Symbol: Prkdc^scid

Genotype: Hc⁰ related

Genotype: Prkdc^scid related

Genotype: Prkdc^scid/Prkdc^scid
NOD.CB17-Prkdc^scid/J

Genotype: Prkdc^scid/Prkdc^scid
NOD.CB17-Prkdc^scid

Additional - Hc⁰ related

Additional - Prkdc^scid related