Strain Name:

NOD.CB17-Prkdcscid/J

Stock Number:

001303

Availability:

Level 1

Common Names: NOD SCID;    
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.

Description

Strain Information

Type Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered Mutant Mice.
Mating SystemHomozygote x Homozygote         (Female x Male)
Specieslaboratory mouse
Background Strain NOD/ShiLtSz
Donor Strain C.BKa-Ighb/IcrSz (C.B-17)
H2 Haplotypeg7
GenerationN10F62 (03-JAN-08)

Appearance
albino
Related Genotype: A/A Tyrc/Tyrc

Description
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.

Development
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/ShiLt background as follows: an NOD/ShiLt 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/ShiLt; at generation N10, Prkdcscid was made homozygous by brother-sister inbreeding.

Control Information

  Control
   001976 NOD/ShiLtJ
   Selection of control mice depends upon the nature of the research.
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Hc0 allele
000645   A/HeJ
000646   A/J
000647   A/WySnJ
000648   AKR/J
000460   B10.D2-Hc0 H2d H2-T18c/o2SnJ
000461   B10.D2-Hc0 H2d H2-T18c/oSnJ
000657   CE/J
000671   DBA/2J
007048   DBA/2J-Gpnmb+/SjJ
001800   FVB/NJ
001491   FVB/NMob
000674   I/LnJ
001976   NOD/ShiLtJ
000684   NZB/BlNJ
000682   RF/J
000688   ST/bJ
000689   SWR/J
View Strains carrying   Hc0     (17 strains)

View Strains carrying   Prkdcscid     (25 strains)

View Strains carrying other alleles of Hc     (5 strains)

Additional Web Information

Congenic Nomenclature
Genetic Quality Control Annual Report
JAX® NOTES, Fall 2003; 491. JAX West Expansion
JAX® NOTES, Fall 2004; 495. NOD.CB17-Prkdcscid/J Strain An Ideal Model for Cancer and Autoimmune Disease.
JAX® NOTES, Spring 1997; 469. Helicobacter Infections in Laboratory Mice.
JAX® NOTES, Spring 1999; 477. Control Strains for NOD/LtJ Mice in Diabetes Research.
JAX® NOTES, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX® NOTES, Spring 2003; 489. Role of NK and NKT Cells in Immunity and Disease.
JAX® NOTES, Spring 2006; 501. Choosing an Immunodeficient Mouse Model.
JAX® NOTES, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX® NOTES, Winter 1999; 476. NOD/LtSz-Prkdcscid/J: An Improved scid Mouse for Cancer and Immunological Research.
JAX® NOTES, Winter 2006; 504. JAX® Mice: the Gold Standard Just Got Better.

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data
Body Weight Information - JAX® Mice Strain NOD.CB17-Prkdcscid/J (001303)
(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)
Mouse Phenome Database
JAX® Physiological Data Summary [pdf]
JAX® Physiological Data Protocol [pdf]
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

Prkdcscid/Prkdcscid

        NOD.CB17-Prkdcscid
  • life span-post-weaning/aging
  • premature death (MGI Ref ID J:22026)
    • average lifespan in SPF housing is 257 days for females and 269 days for males
    • the major cause of death is thymic lymphoma
    • median life span is 37 weeks; death is a result of thymic lymphomas
  • immune system phenotype
  • abnormal lymph organ cellularity (MGI Ref ID J:109833)
    • lymph tissues are severely depleted of lymphoid cells
    • abnormal lymph node cellularity (MGI Ref ID J:22026)
      • lymph nodes lack follicles and consist mostly of stromal cells
      • lymph nodes are hypocellular
    • abnormal thymus cellularity (MGI Ref ID J:109833)
      • lymph nodes are hypocellular
    • spleen hypoplasia (MGI Ref ID J:22026)
      • spleen cellularity is decreased four fold in comparison to NOD control
      • splenic follicles are hypoplastic
  • abnormal response to transplant (MGI Ref ID J:22026)
    • following injection of human T lymphoblastoid cells, 80% of nucleated spleen cells are of human origin by 4 weeks post injection
    • peripheral blood has a five fold increase of human cells by 4 weeks post injection
    • mice support CD34+ human stem cell engraftment, although not as well as mice homozygous for Il2rgtm1Wjl and Prkdcscid
    • 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
    • increased length of allograft survival (MGI Ref ID J:22026)
      • homozygotes (5-6 weeks of age) do not reject orthotopic tail skin allografts throughout a 3 month observation period
  • abnormal spleen white pulp morphology (MGI Ref ID J:22026)
    • splenic follicles exhibit a marked loss of lymphoid cells, however, red pulp is normal
    • splenic follicles are hypoplastic
  • abnormal thymus lobule morphology (MGI Ref ID J:22026)
    • thymic lobes are small and may contain cysts
    • the cortico-medullary junction is not demarcated in tissues from a 10 week old female
  • decreased immunoglobulin level (MGI Ref ID J:22026)
    • 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 (MGI Ref ID J:22026)
  • decreased lymphocyte cell number (MGI Ref ID J:22026)
    • 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 B cell number (MGI Ref ID J:22026)
      • B220+ splenic B cells are decreased (36.0% vs. 10.4%) in comparison to NOD control as measured by flow cytometry
      • decreased mature B cell number (MGI Ref ID J:109833)
        • spleens are deficient in B220+ IgK+ B cells
      • decreased pre-B cell number (MGI Ref ID J:22026)
        • there is a significant absence of splenic B cells bearing the Ig kappa light chain (30.7% vs. 2.8%)
        • B220+ bone marrow pre-B cells are decreased in number (19.0% vs. 10.2%)
    • decreased NK cell number (MGI Ref ID J:22026)
      • no NK1.1+ splenic NK cells were detected by flow cytometry, however some NK cell activity is detected
    • decreased T cell number (MGI Ref ID J:22026)
      • significant numbers of CD3+ splenic T cells are absent in comparison to control (44.9% vs. 0.2%)
      • decreased CD4-positive T cell number (MGI Ref ID J:22026)
        • spleens are deficient in mature T cells
      • decreased CD8-positive T cell number (MGI Ref ID J:22026)
        • spleens are deficient in mature T cells
  • impaired NK cell cytolysis (MGI Ref ID J:22026)
    • NK cell activity in homozygous spleen cell suspensions is markedly decreased in comparison to homozygotes on the CB17 background
  • impaired complement classical pathway (MGI Ref ID J:22026)
    • complement activity is not detected in either homozygous or control sera using a 51Cr-release assay
  • increased granulocyte number (MGI Ref ID J:22026)
    • Gr1+ splenic and bone marrow granulocytes are increased in comparison to control
  • increased macrophage cell number (MGI Ref ID J:22026)
    • F4/80+ splenic macrophages are increased in comparison to control
  • hematopoietic system phenotype
  • abnormal spleen white pulp morphology (MGI Ref ID J:22026)
    • splenic follicles exhibit a marked loss of lymphoid cells, however, red pulp is normal
    • splenic follicles are hypoplastic
  • abnormal thymus cellularity (MGI Ref ID J:109833)
    • lymph nodes are hypocellular
  • abnormal thymus lobule morphology (MGI Ref ID J:22026)
    • thymic lobes are small and may contain cysts
    • the cortico-medullary junction is not demarcated in tissues from a 10 week old female
  • decreased bone marrow cell number (MGI Ref ID J:22026)
    • homozygotes have a 40% reduction in nucleated bone marrow cells compared to NOD control
  • decreased erythrocyte cell number (MGI Ref ID J:22026)
    • homozygotes have significantly reduced erythrocyte counts in contrast to NOD control
  • decreased lymphocyte cell number (MGI Ref ID J:22026)
    • 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 B cell number (MGI Ref ID J:22026)
      • B220+ splenic B cells are decreased (36.0% vs. 10.4%) in comparison to NOD control as measured by flow cytometry
      • decreased mature B cell number (MGI Ref ID J:109833)
        • spleens are deficient in B220+ IgK+ B cells
      • decreased pre-B cell number (MGI Ref ID J:22026)
        • there is a significant absence of splenic B cells bearing the Ig kappa light chain (30.7% vs. 2.8%)
        • B220+ bone marrow pre-B cells are decreased in number (19.0% vs. 10.2%)
    • decreased NK cell number (MGI Ref ID J:22026)
      • no NK1.1+ splenic NK cells were detected by flow cytometry, however some NK cell activity is detected
    • decreased T cell number (MGI Ref ID J:22026)
      • significant numbers of CD3+ splenic T cells are absent in comparison to control (44.9% vs. 0.2%)
      • decreased CD4-positive T cell number (MGI Ref ID J:22026)
        • spleens are deficient in mature T cells
      • decreased CD8-positive T cell number (MGI Ref ID J:22026)
        • spleens are deficient in mature T cells
  • increased granulocyte number (MGI Ref ID J:22026)
    • Gr1+ splenic and bone marrow granulocytes are increased in comparison to control
  • increased macrophage cell number (MGI Ref ID J:22026)
    • F4/80+ splenic macrophages are increased in comparison to control
  • increased mean corpuscular volume (MGI Ref ID J:22026)
    • erythrocyte mean cell volume is elevated in both homozygotes and NOD controls in contrast to homozygotes on the CB17 background
  • spleen hypoplasia (MGI Ref ID J:22026)
    • spleen cellularity is decreased four fold in comparison to NOD control
    • splenic follicles are hypoplastic
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype (MGI Ref ID J:22026)
    • weekly monitoring of urinary glucose demonstrates that mice do not develop diabetes
    • mice do not develop insulitis in contrast to NOD controls
  • tumorigenesis
  • thymic lymphoma (MGI Ref ID J:109833)
    • lymphomas metastasize to multiple sites and are the major cause of death
  • cellular phenotype
  • increased cellular sensitivity to X-ray irradiation (MGI Ref ID J:109833)
    • mice do not survive doses above 400 cGy
    • some irradiated mice exhibit thymic lymphomas or mitotic figures following irradiation
View Research Applications

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

Cancer Research
Increased Tumor Incidence (Lymphomas: thymic)

Diabetes and Obesity Research
Islet Transplantation Studies
Type 1 Diabetes (IDDM) Analysis Strains (NOD Congenics with Mutations Affecting Immunocompetence)

Research Tools
Immunology and Inflammation Research (B and T cell deficiency)

Hc0 related

Immunology and Inflammation Research
Immunodeficiency (specific complement deficiency)

Research Tools
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)

Prkdcscid related

Immunology and Inflammation 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)

Genes & Alleles

Gene & Allele Information

Allele Symbol Prkdcscid
Allele Name severe combined immunodeficiency
Allele Type Spontaneous
Common Name(s) scid;
Strain of OriginCB17
Gene Symbol and Name Prkdc, protein kinase, DNA activated, catalytic polypeptide
Chromosome 16
Gene Common Name(s) AI326420; AU019811; DNA-PK; DNA-PKcs; DNAPDcs; DNAPK; DNPK1; HYRC; HYRC1; MGC189093; XRCC7; expressed sequence AI326420; expressed sequence AU019811; p350; scid; severe combined immunodeficiency; slip;
General Note The Prkdcscid mutation arose in the C.B-17 inbred strain (BALB/c.C57BL/Ka-Igh-1b) (J:9341). Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA, but a few have low levels of one to three of these immunoglobulin isotypes. The size of the lymphoid organs is only one-tenth or less that of normal. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes (J:30980).

Homozygotes are deficient in both B and T cell function. Their spleen cells do not respond to either B or T cell mitogens and they are unable to reject skin grafts. They lack detectable B cells and pre-B cells. In spite of the small thymus and lack of functional T cells, the Thy1 marker is present on a majority of cells recovered from the thymus, and T cell lymphomas occur in 10 per cent or more of affected mice. Prkdcscid specifically impairs differentiation of stem cells into mature lymphocytes. Myeloid cell differentiation is not affected. The basic defect in these mice appears to be in the lymphoid stem cells and not in the cellular environment, since functional T and B cells are found in mice reconstituted with normal bone marrow (J:30980, J:7343). However, full reconstitution of the immune deficiency occurs only after irradiation of the recipients, indicating that Prkdcscid/Prkdcscid mice may have normal numbers of a radiation-sensitive stem cell that has defective proliferative capacity (J:8299).

The rearrangements of immunoglobulin and T cell receptor genes that normally occur in B and T lymphocytes are not found in homozygous Prkdcscid mice. However, in Abelson leukemia virus-transformed B cells of these mice and in their occasional T cell lymphomas, rearrangements, most of which are abnormal, are found. This suggests that scid may act through an effect on the recombinase system catalyzing the assembly of immunoglobulin and T cell receptor genes, and that lymphocytes with these defects are not able to develop further (J:8420).

Although most Prkdcscid homozygotes fail to produce immunoglobulin and functional T-cell receptor, some produce these products at low levels, with an occasional mouse with nearly normal levels of serum immunoglobulin, the criterion usually used tomeasure the effects of Prkdcscid. This phenomenon is referred to as "leakiness" of the VDJ recombination defect (J:4610).Homozygous Prkdcscidmice are fertile and, under specific pathogen-free conditions, may survive a year or more(J:6958).

The Prkdcscid mouse has been widely used in studies of the immune system, in particular of VDJ recombination in T and B lymphocytes. Its lack of immunocompetence has made it useful in transplantation studies, particularly transplantation and development of metastasis in human tumors. The interaction of infection, immunity, and disease processes have been studied with these mice. Poole (J:31292) offers a brief review of the nature and usefulness of the Prkdcscid mouse, with key references to the very extensive literature.

Mutant mRNA does not appear to differ from wild-type although protein expression is reduced more than 10-fold. Mutant protein is defective for nuclear association but exhibits normal DNA-binding ability.

NOD.Cg-Prkdcscid B2mtm1Unc mice lack mature lymphocytes and serum Ig, are MHC class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. These mice display accumulation of iron in the liver and rapid clearance of human IgG1.

Molecular Note A T-to-A transversion point mutation at a position corresponding to codon 4095 created a premature stop codon. [MGI Ref ID J:35393] [MGI Ref ID J:39329]
 
Allele Symbol Hc0
Allele Name deficient
Allele Type Spontaneous
Common Name(s) C5-; C5-d; C5-def; C5-deficient; hco;
Gene Symbol and Name Hc, hemolytic complement
Chromosome 2
Gene Common Name(s) C5; C5a; CPAMD4; FLJ17816; FLJ17822; He; MGC142298; RGD1561905;
General Note

This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, 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, 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. [MGI Ref ID J:23983]

Genotyping

Genotyping Information

Genotyping Protocols

Prkdcscid, PYRO, vers. 2
Prkdcscid, REST, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Selected Reference(s)

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 Ref ID 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 Ref ID J:35393]

Bosma M; Schuler W; Bosma G. 1988. The scid mouse mutant. Curr Top Microbiol Immunol 137:197-202. [PubMed: 3416632]  [MGI Ref ID 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 Ref ID J:34990]

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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:69909]

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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:71651]

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 Ref ID 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 Ref ID J:107269]

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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 Ref ID J:94347]

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 Ref ID J:138026]

Borders CW; Courtney A; Ronen K; Pilar Laborde-Lahoz M; Guidry TV; Hwang SA; Olsen M; Hunter RL Jr; Hollmann TJ; Wetsel RA; Actor JK. 2005. Requisite role for complement C5 and the C5a receptor in granulomatous response to mycobacterial glycolipid trehalose 6,6'-dimycolate. Scand J Immunol 62(2):123-30. [PubMed: 16101818]  [MGI Ref ID J:114316]

Carter WO; Bull C; Bortolon E; Yang L; Jesmok GJ; Gundel RH. 1998. A murine skeletal muscle ischemia-reperfusion injury model: differential pathology in BALB/c and DBA/2N mice. J Appl Physiol 85(5):1676-83. [PubMed: 9804569]  [MGI Ref ID J:51187]

Chen J; Reifsnyder PC; Scheuplein F; Schott WH; Mileikovsky M; Soodeen-Karamath S; Nagy A; Dosch MH; Ellis J; Koch-Nolte F; Leiter EH. 2005. 'Agouti NOD': identification of a CBA-derived Idd locus on Chromosome 7 and its use for chimera production with NOD embryonic stem cells. Mamm Genome 16(10):775-83. [PubMed: 16261419]  [MGI Ref ID J:102639]

Cunnion KM; Benjamin DK Jr; Hester CG; Frank MM. 2004. Role of complement receptors 1 and 2 (CD35 and CD21), C3, C4, and C5 in survival by mice of Staphylococcus aureus bacteremia. J Lab Clin Med 143(6):358-65. [PubMed: 15192652]  [MGI Ref ID J:101948]

Daniel DS; Dai G; Singh CR; Lindsey DR; Smith AK; Dhandayuthapani S; Hunter RL Jr; Jagannath C. 2006. The reduced bactericidal function of complement C5-deficient murine macrophages is associated with defects in the synthesis and delivery of reactive oxygen radicals to mycobacterial phagosomes. J Immunol 177(7):4688-98. [PubMed: 16982908]  [MGI Ref ID J:139313]

Deguchi Y; Andoh A; Inatomi O; Araki Y; Hata K; Tsujikawa T; Kitoh K; Fujiyama Y. 2005. Development of dextran sulfate sodium-induced colitis is aggravated in mice genetically deficient for complement C5. Int J Mol Med 16(4):605-8. [PubMed: 16142393]  [MGI Ref ID J:107581]

Fairweather D; Frisancho-Kiss S; Njoku DB; Nyland JF; Kaya Z; Yusung SA; Davis SE; Frisancho JA; Barrett MA; Rose NR. 2006. Complement receptor 1 and 2 deficiency increases coxsackievirus B3-induced myocarditis, dilated cardiomyopathy, and heart failure by increasing macrophages, IL-1beta, and immune complex deposition in the heart. J Immunol 176(6):3516-24. [PubMed: 16517720]  [MGI Ref ID J:129509]

Flierl MA; Rittirsch D; Nadeau BA; Day DE; Zetoune FS; Sarma JV; Huber-Lang MS; Ward PA. 2008. Functions of the complement components C3 and C5 during sepsis. FASEB J 22(10):3483-90. [PubMed: 18587006]  [MGI Ref ID J:140250]

Girardi G; Berman J; Redecha P; Spruce L; Thurman JM; Kraus D; Hollmann TJ; Casali P; Caroll MC; Wetsel RA; Lambris JD; Holers VM; Salmon JE. 2003. Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. J Clin Invest 112(11):1644-54. [PubMed: 14660741]  [MGI Ref ID J:86845]

Hillebrandt S; Wasmuth HE; Weiskirchen R; Hellerbrand C; Keppeler H; Werth A; Schirin-Sokhan R; Wilkens G; Geier A; Lorenzen J; Kohl J; Gressner AM; Matern S; Lammert F. 2005. Complement factor 5 is a quantitative trait gene that modifies liver fibrogenesis in mice and humans. Nat Genet 37(8):835-43. [PubMed: 15995705]  [MGI Ref ID J:100159]

Karp CL; Grupe A; Schadt E; Ewart SL; Keane-Moore M; Cuomo PJ; Kohl J; Wahl L; Kuperman D; Germer S; Aud D; Peltz G; Wills-Karp M. 2000. Identification of complement factor 5 as a susceptibility locus for experimental allergic asthma. Nat Immunol 1(3):221-6. [PubMed: 10973279]  [MGI Ref ID J:108211]

Kawikova I; Paliwal V; Szczepanik M; Itakura A; Fukui M; Campos RA; Geba GP; Homer RJ; Iliopoulou BP; Pober JS; Tsuji RF; Askenase PW. 2004. Airway hyper-reactivity mediated by B-1 cell immunoglobulin M antibody generating complement C5a at 1 day post-immunization in a murine hapten model of non-atopic asthma. Immunology 113(2):234-45. [PubMed: 15379984]  [MGI Ref ID J:92933]

Kerepesi LA; Hess JA; Nolan TJ; Schad GA; Abraham D. 2006. Complement component C3 is required for protective innate and adaptive immunity to larval strongyloides stercoralis in mice. J Immunol 176(7):4315-22. [PubMed: 16547268]  [MGI Ref ID J:129872]

Kim DD; Miwa T; Kimura Y; Schwendener RA; van Lookeren Campagne M; Song WC. 2008. Deficiency of decay-accelerating factor and complement receptor 1-related gene/protein y on murine platelets leads to complement-dependent clearance by the macrophage phagocytic receptor CRIg. Blood 112(4):1109-19. [PubMed: 18524992]  [MGI Ref ID J:138410]

Kirimanjeswara GS; Mann PB; Pilione M; Kennett MJ; Harvill ET. 2005. The complex mechanism of antibody-mediated clearance of Bordetella from the lungs requires TLR4. J Immunol 175(11):7504-11. [PubMed: 16301658]  [MGI Ref ID J:122156]

Kyriakides C; Austen W Jr; Wang Y; Favuzza J; Kobzik L; Moore FD Jr; Hechtman HB. 1999. Membrane attack complex of complement and neutrophils mediate the injury of acid aspiration. J Appl Physiol 87(6):2357-61. [PubMed: 10601189]  [MGI Ref ID J:103341]

Mahesh J; Daly J; Cheadle WG; Kotwal GJ. 1999. Elucidation of the early events contributing to zymosan-induced multiple organ dysfunction syndrome using MIP-1alpha, C3 knockout, and C5-deficient mice. Shock 12(5):340-9. [PubMed: 10565608]  [MGI Ref ID J:59655]

Mastellos D; Papadimitriou JC; Franchini S; Tsonis PA; Lambris JD. 2001. A novel role of complement: mice deficient in the fifth component of complement (C5) exhibit impaired liver regeneration. J Immunol 166(4):2479-86. [PubMed: 11160308]  [MGI Ref ID J:111000]

Miller CG; Cook DN; Kotwal GJ. 1996. Two chemotactic factors, C5a and MIP-1alpha, dramatically alter the mortality from zymosan-induced multiple organ dysfunction syndrome (MODS): C5a contributes to MODS while MIP-1alpha has a protective role. Mol Immunol 33(14):1135-7. [PubMed: 9047380]  [MGI Ref ID J:38592]

Miller CG; Justus DE; Jayaraman S; Kotwal GJ. 1995. Severe and prolonged inflammatory response to localized cowpox virus infection in footpads of C5-deficient mice: investigation of the role of host complement in poxvirus pathogenesis. Cell Immunol 162(2):326-32. [PubMed: 7743560]  [MGI Ref ID J:25289]

Mocco J; Mack WJ; Ducruet AF; Sosunov SA; Sughrue ME; Hassid BG; Nair MN; Laufer I; Komotar RJ; Claire M; Holland H; Pinsky DJ; Connolly ES Jr. 2006. Complement component C3 mediates inflammatory injury following focal cerebral ischemia. Circ Res 99(2):209-17. [PubMed: 16778128]  [MGI Ref ID J:123658]

Mori L; de Libero G. 1998. Genetic control of susceptibility to collagen-induced arthritis in T cell receptor beta-chain transgenic mice. Arthritis Rheum 41(2):256-62. [PubMed: 9485083]  [MGI Ref ID J:134111]

Moulton RA; Mashruwala MA; Smith AK; Lindsey DR; Wetsel RA; Haviland DL; Hunter RL; Jagannath C. 2007. Complement C5a anaphylatoxin is an innate determinant of dendritic cell-induced Th1 immunity to Mycobacterium bovis BCG infection in mice. J Leukoc Biol 82(4):956-67. [PubMed: 17675563]  [MGI Ref ID J:125190]

Mullick A; Elias M; Picard S; Bourget L; Jovcevski O; Gauthier S; Tuite A; Harakidas P; Bihun C; Massie B; Gros P. 2004. Dysregulated inflammatory response to Candida albicans in a C5-deficient mouse strain. Infect Immun 72(10):5868-76. [PubMed: 15385488]  [MGI Ref ID J:93132]

Mullick A; Leon Z; Min-Oo G; Berghout J; Lo R; Daniels E; Gros P. 2006. Cardiac failure in C5-deficient A/J mice after Candida albicans infection. Infect Immun 74(8):4439-51. [PubMed: 16861630]  [MGI Ref ID J:112405]

Niculescu T; Weerth S; Niculescu F; Cudrici C; Rus V; Raine CS; Shin ML; Rus H. 2004. Effects of complement C5 on apoptosis in experimental autoimmune encephalomyelitis. J Immunol 172(9):5702-6. [PubMed: 15100315]  [MGI Ref ID J:89686]

Nilsson UR; Muller-Eberhard HJ. 1967. Deficiency of the fifth component of complement in mice with an inherited complement defect. J Exp Med 125(1):1-16. [PubMed: 4959665]  [MGI Ref ID J:5016]

Ooi YM; Colten HR. 1979. Genetic defect in secretion of complement C5 in mice. Nature 282(5735):207-8. [PubMed: 492335]  [MGI Ref ID J:6214]

Patel SN; Berghout J; Lovegrove FE; Ayi K; Conroy A; Serghides L; Min-oo G; Gowda DC; Sarma JV; Rittirsch D; Ward PA; Liles WC; Gros P; Kain KC. 2008. C5 deficiency and C5a or C5aR blockade protects against cerebral malaria. J Exp Med 205(5):1133-43. [PubMed: 18426986]  [MGI Ref ID J:136298]

Pickering MC; Warren J; Rose KL; Carlucci F; Wang Y; Walport MJ; Cook HT; Botto M. 2006. Prevention of C5 activation ameliorates spontaneous and experimental glomerulonephritis in factor H-deficient mice. Proc Natl Acad Sci U S A 103(25):9649-54. [PubMed: 16769899]  [MGI Ref ID J:111031]

Pilione MR; Agosto LM; Kennett MJ; Harvill ET. 2006. CD11b is required for the resolution of inflammation induced by Bordetella bronchiseptica respiratory infection. Cell Microbiol 8(5):758-68. [PubMed: 16611225]  [MGI Ref ID J:135740]

Pritchard MT; McMullen MR; Stavitsky AB; Cohen JI; Lin F; Medof ME; Nagy LE. 2007. Differential contributions of C3, C5, and decay-accelerating factor to ethanol-induced fatty liver in mice. Gastroenterology 132(3):1117-26. [PubMed: 17383432]  [MGI Ref ID J:128218]

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Refici ML; Metzger DW; Arulanandam BP; Lennartz MR; Loegering DJ. 2001. Fcgamma-receptor signaling augments the LPS-stimulated increase in serum tumor necrosis factor-alpha levels. Am J Physiol Regul Integr Comp Physiol 280(4):R1037-44. [PubMed: 11247825]  [MGI Ref ID J:114295]

Rittirsch D; Flierl MA; Day DE; Nadeau BA; McGuire SR; Hoesel LM; Ipaktchi K; Zetoune FS; Sarma JV; Leng L; Huber-Lang MS; Neff TA; Bucala R; Ward PA. 2008. Acute lung injury induced by lipopolysaccharide is independent of complement activation. J Immunol 180(11):7664-72. [PubMed: 18490769]  [MGI Ref ID J:136379]

Rittirsch D; Flierl MA; Nadeau BA; Day DE; Huber-Lang M; Mackay CR; Zetoune FS; Gerard NP; Cianflone K; Kohl J; Gerard C; Sarma JV; Ward PA. 2008. Functional roles for C5a receptors in sepsis. Nat Med 14(5):551-7. [PubMed: 18454156]  [MGI Ref ID J:136703]

Saville SP; Lazzell AL; Chaturvedi AK; Monteagudo C; Lopez-Ribot JL. 2008. Use of a genetically engineered strain to evaluate the pathogenic potential of yeast cell and filamentous forms during Candida albicans systemic infection in immunodeficient mice. Infect Immun 76(1):97-102. [PubMed: 17967861]  [MGI Ref ID J:130296]

Sood R; Sholl L; Isermann B; Zogg M; Coughlin SR; Weiler H. 2008. Maternal Par4 and platelets contribute to defective placenta formation in mouse embryos lacking thrombomodulin. Blood 112(3):585-91. [PubMed: 18490515]  [MGI Ref ID J:138440]

Stokol T; O'Donnell P; Xiao L; Knight S; Stavrakis G; Botto M; von Andrian UH; Mayadas TN. 2004. C1q governs deposition of circulating immune complexes and leukocyte Fcgamma receptors mediate subsequent neutrophil recruitment. J Exp Med 200(7):835-46. [PubMed: 15466618]  [MGI Ref ID J:93949]

Strainic MG; Liu J; Huang D; An F; Lalli PN; Muqim N; Shapiro VS; Dubyak GR; Heeger PS; Medof ME. 2008. Locally produced complement fragments C5a and C3a provide both costimulatory and survival signals to naive CD4+ T cells. Immunity 28(3):425-35. [PubMed: 18328742]  [MGI Ref ID J:132942]

Strey CW; Markiewski M; Mastellos D; Tudoran R; Spruce LA; Greenbaum LE; Lambris JD. 2003. The proinflammatory mediators C3a and C5a are essential for liver regeneration. J Exp Med 198(6):913-23. [PubMed: 12975457]  [MGI Ref ID J:109380]

Tanaka D; Kagari T; Doi H; Shimozato T. 2006. Essential role of neutrophils in anti-type II collagen antibody and lipopolysaccharide-induced arthritis. Immunology 119(2):195-202. [PubMed: 16836650]  [MGI Ref ID J:118551]

Trendelenburg M; Fossati-Jimack L; Cortes-Hernandez J; Turnberg D; Lewis M; Izui S; Cook HT; Botto M. 2005. The role of complement in cryoglobulin-induced immune complex glomerulonephritis. J Immunol 175(10):6909-14. [PubMed: 16272350]  [MGI Ref ID J:119691]

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Prkdcscid related

Ahsmann EJ; van Tol MJ; Oudeman-Gruber J; Lokhorst H; Uytdehaag FG; Schuurman HJ; Bloem AC. 1995. The SCID mouse as a model for multiple myeloma. Br J Haematol 89(2):319-27. [PubMed: 7873382]  [MGI Ref ID J:22989]

Akiba H; Takeda K; Kojima Y; Usui Y; Harada N; Yamazaki T; Ma J; Tezuka K; Yagita H; Okumura K. 2005. The role of ICOS in the CXCR5+ follicular B helper T cell maintenance in vivo. J Immunol 175(4):2340-8. [PubMed: 16081804]  [MGI Ref ID J:107507]

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Anderson MG; Nair KS; Amonoo LA; Mehalow A; Trantow CM; Masli S; John SW. 2008. GpnmbR150X allele must be present in bone marrow derived cells to mediate DBA/2J glaucoma. BMC Genet 9:30. [PubMed: 18402690]  [MGI Ref ID J:134670]

Andoh M; Zhang G; Russell-Lodrigue KE; Shive HR; Weeks BR; Samuel JE. 2007. T Cells Are Essential for Bacterial Clearance, and Gamma Interferon, Tumor Necrosis Factor Alpha, and B Cells Are Crucial for Disease Development in Coxiella burnetii Infection in Mice. Infect Immun 75(7):3245-55. [PubMed: 17438029]  [MGI Ref ID J:122426]

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