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The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names NOD.B6-Pfptm1Sdz    (Changed: 15-DEC-04 )
Type Congenic; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain NOD/ShiLt
Donor Strain C57BL/6 via B6III ES cell line
H2 Haplotypeg7
Donating InvestigatorDr. David Kagi,   Ontario Cancer Institute, Rm8-622

albino, pink eyed
Related Genotype: A/A Tyrc/Tyrc

Mice homozygous for the Prf1tm1Sdz targeted mutation are viable and fertile. Homozygous mutant mice on an autoimmune type 1 diabetes prone NOD background have normal numbers of CD4- CD8+ T cells in the spleen. CD4- CD8- expressing T lymphocytes were also normal. NOD mice show a progressive infilitatraion of mononuclear cells into pancreatic islets beginning around 5 weeks of age. NOD wildtype and PRF1 deficient mice show similar development of insulititis. However, disease incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age. These results show the importance of perforin-mediated cytotoxic T cells in development of autoimmune diabetes. (Kagi et al., 1994; Kagi et al., 1997.)

The endogenous perforin (Prf1) gene was disrupted by the insertion of a targeting construct into the third exon of the gene without deletion of coding sequence. The 3.3 kb targeting construct consisted of exon 3, a portion of the preceding intron, and a selective neomycin resistance cassette. Positive BL/6III ES cells (derived from C57BL/6), as determined by Southern Blot analysis, were injected into BALB/c blastocysts. Chimeric mice were bred with C57BL/6 to create individuals heterozygous for the disrupted Prf1 gene, which were then intercrossed to obtain homozygous mutant mice on the C57BL/6 background (Stock# 002407). Homozygous mutant mice were confirmed to lack the PRF1 protein by the absence of PRF1 antibody staining of stimulated spleen cells. The mutation was transferred to the NOD background via at least seven backcrosses after which heterozygous individuals were intercrossed to produce homozygous mutant mice on the NOD background. This strain has been maintained by sibling mating homozygous mice. (Kagi et al., 1994; Kagi et al., 1997.)

Control Information

   See control note: Additional control strains are available depending on the researchers needs. Please refer to JAX Notes No. 477 for a complete list of control strains available for NOD/LtJ mice in diabetes research. JAX Notes .
   001976 NOD/ShiLtJ
  Considerations for Choosing Controls

Related Strains

Strains carrying   Prf1tm1Sdz allele
002407   C57BL/6-Prf1tm1Sdz/J
007079   CByJ.B6-Prf1tm1Sdz/J
008659   NOD.Cg-Rag1tm1Mom Ins2Akita Prf1tm1Sdz/SzJ
004848   NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/SzJ
View Strains carrying   Prf1tm1Sdz     (4 strains)


Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Aplastic Anemia   (PRF1)
Hemophagocytic Lymphohistiocytosis, Familial, 2; FHL2   (PRF1)
Lymphoma, Non-Hodgkin, Familial   (PRF1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype


  • immune system phenotype
  • decreased susceptibility to autoimmune diabetes
    • female heterozygous NOD mice show a delayed incidence (median: week 27) in development of diabetes (determined by high blood glucose) with an incidence of 67% compared to early onset (median: week 19) with an incidence of 77% in control NOD mice   (MGI Ref ID J:43468)
  • insulitis
    • at 8 weeks of age, insulitis is seen to varying degrees in perforin-null and heterozygous mice; by 55 weeks of age, in non-diabetic null mice, severe insulitis develops with a higher frequency than in perforin- expressing NOD controls   (MGI Ref ID J:43468)
  • periinsulitis
    • periinsulitis is observed in 8-week old perforin-null and heterozygous mice with little islet cell damage, compared to detection at 5 weeks in control NOD mice   (MGI Ref ID J:43468)
  • endocrine/exocrine gland phenotype
  • insulitis
    • at 8 weeks of age, insulitis is seen to varying degrees in perforin-null and heterozygous mice; by 55 weeks of age, in non-diabetic null mice, severe insulitis develops with a higher frequency than in perforin- expressing NOD controls   (MGI Ref ID J:43468)
  • periinsulitis
    • periinsulitis is observed in 8-week old perforin-null and heterozygous mice with little islet cell damage, compared to detection at 5 weeks in control NOD mice   (MGI Ref ID J:43468)


  • homeostasis/metabolism phenotype
  • abnormal circulating glucose level
    • after cyclophosphamide treatment, perforin-null NOD mice display temporary hyperglycemia but return to normoglycemia while control NOD mice become hyperglycemic and often die as a result   (MGI Ref ID J:43468)
  • increased physiological sensitivity to xenobiotic
    • cyclophosphamide treatment of 8-12 week old NOD control and perforin-heterozygous NOD mice on day 0 and 12 induces diabetes at an incidence of 80-90% after the second treatment between 24 and 30 days, while diabetes occurs in 18% of homozygous NOD mutants between 32 and 38 days   (MGI Ref ID J:43468)
  • endocrine/exocrine gland phenotype
  • decreased pancreatic beta cell number
    • diabetic perforin-null mice have a drastically reduced volume density of endocrine islet tissue (beta cells) compared with 7-week old control NOD mice   (MGI Ref ID J:43468)
  • insulitis
    • at 8 weeks of age, insulitis is seen to varying degrees in perforin-null and heterozygous mice; by 55 weeks of age, in non-diabetic null mice, severe insulitis develops with a higher frequency than in perforin-expressing NOD controls   (MGI Ref ID J:43468)
  • periinsulitis
    • periinsulitis is observed in 8-week old perforin-null and heterozygous mice with little islet cell damage, compared to detection at 5 weeks in control NOD mice   (MGI Ref ID J:43468)
  • immune system phenotype
  • decreased susceptibility to autoimmune diabetes
    • female perforin-null NOD mice show significantly decrease incidence of diabetes (16%) with a delayed onset between 35 and 41 weeks, while control NOD mice, diabetes occurred between 15 and 30 weeks of age with an incidence of 77%; male control NOD mice show less than 20% incidence of diabetes, while no null NOD mice develop diabetes   (MGI Ref ID J:43468)
  • insulitis
    • at 8 weeks of age, insulitis is seen to varying degrees in perforin-null and heterozygous mice; by 55 weeks of age, in non-diabetic null mice, severe insulitis develops with a higher frequency than in perforin-expressing NOD controls   (MGI Ref ID J:43468)
  • periinsulitis
    • periinsulitis is observed in 8-week old perforin-null and heterozygous mice with little islet cell damage, compared to detection at 5 weeks in control NOD mice   (MGI Ref ID J:43468)
View Research Applications

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

Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains
      NOD Congenics with Mutations Affecting Cytokine Production by Autoreactive T Cells

Prf1tm1Sdz related

Apoptosis Research
Extracellular Modulators

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Prf1tm1Sdz
Allele Name targeted mutation 1, Sandoz Pharmaceuticals
Allele Type Targeted (Null/Knockout)
Common Name(s) P0; Pfn-; Pfptm1Sdz; Prf1-; Prf1tm/Sdz; Prf-; perf-; perforin 0; perforin-; pfp-; pfpKO; pko; prf1tm1;
Mutation Made ByDr. Birgit Lederman,   University of Zurich
Strain of OriginC57BL/6J
ES Cell Line NameBL/6-III
ES Cell Line StrainC57BL/6J
Gene Symbol and Name Prf1, perforin 1 (pore forming protein)
Chromosome 10
Gene Common Name(s) Cyta; FLH2; HPLH2; P1; PFN1; PFP; Pfn; Pfp; Prf-1; RATCYTA; perforin; perforin 1; pore forming protein;
General Note Phenotypic Similarity to Human Syndrome: hemophagocytic lymphohistiocytosis in mutants infected with lymphocytic choriomeningitic virus (J:92260)
Molecular Note A neomycin selection cassette was inserted into exon 3. RT-PCR analysis on RNA derived from homozygous mice demonstrated that an abnormal transcript was produced from this allele. However, immunocytochemistry experiments on activated spleen cells derived from homozygous mice confirmed that no detectable protein was made from this allele. [MGI Ref ID J:17986] [MGI Ref ID J:96542]


Genotyping Information

Genotyping Protocols

Prf1tm1Sdz, High Resolution Melting
Prf1tm1Sdz, Standard PCR

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Selected Reference(s)

Kagi D; Odermatt B; Seiler P; Zinkernagel RM; Mak TW; Hengartner H. 1997. Reduced incidence and delayed onset of diabetes in perforin-deficient nonobese diabetic mice. J Exp Med 186(7):989-97. [PubMed: 9314549]  [MGI Ref ID J:43468]

Additional References

Kwon BS; Wakulchik M; Liu CC; Persechini PM; Trapani JA; Haq AK; Kim Y; Young JD. 1989. The structure of the mouse lymphocyte pore-forming protein perforin. Biochem Biophys Res Commun 158(1):1-10. [PubMed: 2783549]  [MGI Ref ID J:9554]

Lichtenheld MG; Podack ER. 1992. Structure and function of the murine perforin promoter and upstream region. Reciprocal gene activation or silencing in perforin positive and negative cells. J Immunol 149(8):2619-26. [PubMed: 1401900]  [MGI Ref ID J:2869]

Lowrey DM; Aebischer T; Olsen K; Lichtenheld M; Rupp F; Hengartner H; Podack ER. 1989. Cloning, analysis, and expression of murine perforin 1 cDNA, a component of cytolytic T-cell granules with homology to complement component C9. Proc Natl Acad Sci U S A 86(1):247-51. [PubMed: 2783486]  [MGI Ref ID J:9549]

Trapani JA; Kwon BS; Kozak CA; Chintamaneni C; Young JD; Dupont B. 1990. Genomic organization of the mouse pore-forming protein (perforin) gene and localization to chromosome 10. Similarities to and differences from C9. J Exp Med 171(2):545-57. [PubMed: 2303785]  [MGI Ref ID J:10315]

Prf1tm1Sdz related

Abdool K; Cretney E; Brooks AD; Kelly JM; Swann J; Shanker A; Bere EW Jr; Yokoyama WM; Ortaldo JR; Smyth MJ; Sayers TJ. 2006. NK cells use NKG2D to recognize a mouse renal cancer (Renca), yet require intercellular adhesion molecule-1 expression on the tumor cells for optimal perforin-dependent effector function. J Immunol 177(4):2575-83. [PubMed: 16888019]  [MGI Ref ID J:138353]

Afshar-Sterle S; Zotos D; Bernard NJ; Scherger AK; Rodling L; Alsop AE; Walker J; Masson F; Belz GT; Corcoran LM; O'Reilly LA; Strasser A; Smyth MJ; Johnstone R; Tarlinton DM; Nutt SL; Kallies A. 2014. Fas ligand-mediated immune surveillance by T cells is essential for the control of spontaneous B cell lymphomas. Nat Med 20(3):283-90. [PubMed: 24487434]  [MGI Ref ID J:208773]

Alsharifi M; Lobigs M; Simon MM; Kersten A; Muller K; Koskinen A; Lee E; Mullbacher A. 2006. NK cell-mediated immunopathology during an acute viral infection of the CNS. Eur J Immunol 36(4):887-96. [PubMed: 16541469]  [MGI Ref ID J:114787]

Alves B; Leong J; Tamang DL; Elliott V; Lowe M; Hudig D. 2009. Hydrolysis of tumor cell lipids after CTL-mediated death. Int Immunol 21(5):543-53. [PubMed: 19325035]  [MGI Ref ID J:148103]

Alves BN; Leong J; Tamang DL; Elliott V; Edelnant J; Redelman D; Singer CA; Kuhn AR; Miller R; Lowe ME; Hudig D. 2009. Pancreatic lipase-related protein 2 (PLRP2) induction by IL-4 in cytotoxic T lymphocytes (CTLs) and reevaluation of the negative effects of its gene ablation on cytotoxicity. J Leukoc Biol 86(3):701-12. [PubMed: 19451396]  [MGI Ref ID J:152431]

Anthony DA; Andrews DM; Chow M; Watt SV; House C; Akira S; Bird PI; Trapani JA; Smyth MJ. 2010. A role for granzyme M in TLR4-driven inflammation and endotoxicosis. J Immunol 185(3):1794-803. [PubMed: 20585036]  [MGI Ref ID J:162467]

Ataera H; Simkins HM; Hyde E; Yang J; Hermans IF; Petersen TR; Ronchese F. 2013. The control of CD8+ T cell responses is preserved in perforin-deficient mice and released by depletion of CD4+CD25+ regulatory T cells. J Leukoc Biol 94(4):825-33. [PubMed: 23883515]  [MGI Ref ID J:205311]

Baker MB; Altman NH; Podack ER; Levy RB. 1996. The role of cell-mediated cytotoxicity in acute GVHD after MHC-matched allogeneic bone marrow transplantation in mice. J Exp Med 183(6):2645-56. [PubMed: 8676085]  [MGI Ref ID J:33612]

Balkow S; Kersten A; Tran TT; Stehle T; Grosse P; Museteanu C; Utermohlen O; Pircher H; von Weizsacker F; Wallich R; Mullbacher A; Simon MM. 2001. Concerted action of the FasL/Fas and perforin/granzyme A and B pathways is mandatory for the development of early viral hepatitis but not for recovery from viral infection. J Virol 75(18):8781-91. [PubMed: 11507223]  [MGI Ref ID J:71217]

Ballas ZK; Buchta CM; Rosean TR; Heusel JW; Shey MR. 2013. Role of NK cell subsets in organ-specific murine melanoma metastasis. PLoS One 8(6):e65599. [PubMed: 23776508]  [MGI Ref ID J:204234]

Banuelos SJ; Shultz LD; Greiner DL; Burzenski LM; Gott B; Lyons BL; Rossini AA; Appel MC. 2004. Rejection of human islets and human HLA-A2.1 transgenic mouse islets by alloreactive human lymphocytes in immunodeficient NOD-scid and NOD-Rag1(null)Prf1(null) mice. Clin Immunol 112(3):273-83. [PubMed: 15308121]  [MGI Ref ID J:91764]

Beilke JN; Kuhl NR; Van Kaer L; Gill RG. 2005. NK cells promote islet allograft tolerance via a perforin-dependent mechanism. Nat Med 11(10):1059-65. [PubMed: 16155578]  [MGI Ref ID J:101693]

Bitsaktsis C; Winslow G. 2006. Fatal recall responses mediated by CD8 T cells during intracellular bacterial challenge infection. J Immunol 177(7):4644-51. [PubMed: 16982903]  [MGI Ref ID J:139316]

Blazar BR; Carreno BM; Panoskaltsis-Mortari A; Carter L; Iwai Y; Yagita H; Nishimura H; Taylor PA. 2003. Blockade of programmed death-1 engagement accelerates graft-versus-host disease lethality by an IFN-gamma-dependent mechanism. J Immunol 171(3):1272-7. [PubMed: 12874215]  [MGI Ref ID J:120213]

Blazar BR; Lees CJ; Martin PJ; Noelle RJ; Kwon B; Murphy W; Taylor PA. 2000. Host T cells resist graft-versus-host disease mediated by donor leukocyte infusions. J Immunol 165(9):4901-9. [PubMed: 11046015]  [MGI Ref ID J:118027]

Blohm U; Potthoff D; van der Kogel AJ; Pircher H. 2006. Solid tumors 'melt' from the inside after successful CD8 T cell attack. Eur J Immunol 36(2):468-77. [PubMed: 16385625]  [MGI Ref ID J:113858]

Bokhari SM; Kim KJ; Pinson DM; Slusser J; Yeh HW; Parmely MJ. 2008. NK cells and gamma interferon coordinate the formation and function of hepatic granulomas in mice infected with the Francisella tularensis live vaccine strain. Infect Immun 76(4):1379-89. [PubMed: 18227174]  [MGI Ref ID J:133531]

Bolitho P; Street SE; Westwood JA; Edelmann W; Macgregor D; Waring P; Murray WK; Godfrey DI; Trapani JA; Johnstone RW; Smyth MJ. 2009. Perforin-mediated suppression of B-cell lymphoma. Proc Natl Acad Sci U S A 106(8):2723-8. [PubMed: 19196996]  [MGI Ref ID J:146488]

Bour-Jordan H; Thompson HL; Bluestone JA. 2005. Distinct effector mechanisms in the development of autoimmune neuropathy versus diabetes in nonobese diabetic mice. J Immunol 175(9):5649-55. [PubMed: 16237054]  [MGI Ref ID J:119359]

Brien JD; Uhrlaub JL; Nikolich-Zugich J. 2008. West nile virus-specific CD4 T cells exhibit direct antiviral cytokine secretion and cytotoxicity and are sufficient for antiviral protection. J Immunol 181(12):8568-75. [PubMed: 19050276]  [MGI Ref ID J:142059]

Bucher C; Koch L; Vogtenhuber C; Goren E; Munger M; Panoskaltsis-Mortari A; Sivakumar P; Blazar BR. 2009. IL-21 blockade reduces graft-versus-host disease mortality by supporting inducible T regulatory cell generation. Blood 114(26):5375-84. [PubMed: 19843883]  [MGI Ref ID J:155701]

Capitini CM; Nasholm NM; Duncan BB; Guimond M; Fry TJ. 2013. Graft-versus-host disease impairs vaccine responses through decreased CD4+ and CD8+ T cell proliferation and increased perforin-mediated CD8+ T cell apoptosis. J Immunol 190(3):1351-9. [PubMed: 23275602]  [MGI Ref ID J:193034]

Chamberlain CM; Ang LS; Boivin WA; Cooper DM; Williams SJ; Zhao H; Hendel A; Folkesson M; Swedenborg J; Allard MF; McManus BM; Granville DJ. 2010. Perforin-independent extracellular granzyme B activity contributes to abdominal aortic aneurysm. Am J Pathol 176(2):1038-49. [PubMed: 20035050]  [MGI Ref ID J:156606]

Chan CJ; Andrews DM; McLaughlin NM; Yagita H; Gilfillan S; Colonna M; Smyth MJ. 2010. DNAM-1/CD155 interactions promote cytokine and NK cell-mediated suppression of poorly immunogenic melanoma metastases. J Immunol 184(2):902-11. [PubMed: 20008292]  [MGI Ref ID J:159408]

Chang E; Galle L; Maggs D; Estes DM; Mitchell WJ. 2000. Pathogenesis of herpes simplex virus type 1-induced corneal inflammation in perforin-deficient mice J Virol 74(24):11832-40. [PubMed: 11090183]  [MGI Ref ID J:65895]

Chatterjee S; Eby JM; Al-Khami AA; Soloshchenko M; Kang HK; Kaur N; Naga OS; Murali A; Nishimura MI; Le Poole IC; Mehrotra S. 2014. A quantitative increase in regulatory T cells controls development of vitiligo. J Invest Dermatol 134(5):1285-94. [PubMed: 24366614]  [MGI Ref ID J:208054]

Chaudhri G; Tahiliani V; Eldi P; Karupiah G. 2015. Vaccine-induced protection against orthopoxvirus infection is mediated through the combined functions of CD4 T cell-dependent antibody and CD8 T cell responses. J Virol 89(3):1889-99. [PubMed: 25428875]  [MGI Ref ID J:222475]

Chen L; Woo M; Hakem R; Miller RG. 2003. Perforin-dependent activation-induced cell death acts through caspase 3 but not through caspases 8 or 9. Eur J Immunol 33(3):769-78. [PubMed: 12616497]  [MGI Ref ID J:82433]

Chen M; Felix K; Wang J. 2012. Critical role for perforin and Fas-dependent killing of dendritic cells in the control of inflammation. Blood 119(1):127-36. [PubMed: 22042696]  [MGI Ref ID J:181665]

Chen M; Felix K; Wang J. 2011. Immune regulation through mitochondrion-dependent dendritic cell death induced by T regulatory cells. J Immunol 187(11):5684-92. [PubMed: 22031758]  [MGI Ref ID J:179762]

Chen M; Wang YH; Wang Y; Huang L; Sandoval H; Liu YJ; Wang J. 2006. Dendritic cell apoptosis in the maintenance of immune tolerance. Science 311(5764):1160-4. [PubMed: 16497935]  [MGI Ref ID J:105747]

Chiarle R; Martinengo C; Mastini C; Ambrogio C; D'Escamard V; Forni G; Inghirami G. 2008. The anaplastic lymphoma kinase is an effective oncoantigen for lymphoma vaccination. Nat Med 14(6):676-80. [PubMed: 18469826]  [MGI Ref ID J:136968]

Cho HI; Celis E. 2009. Optimized peptide vaccines eliciting extensive CD8 T-cell responses with therapeutic antitumor effects. Cancer Res 69(23):9012-9. [PubMed: 19903852]  [MGI Ref ID J:155054]

Choi J; Ritchey J; Prior JL; Holt M; Shannon WD; Deych E; Piwnica-Worms DR; DiPersio JF. 2010. In vivo administration of hypomethylating agents mitigate graft-versus-host disease without sacrificing graft-versus-leukemia. Blood 116(1):129-39. [PubMed: 20424188]  [MGI Ref ID J:162801]

Chong SZ; Tan KW; Wong FH; Chua YL; Tang Y; Ng LG; Angeli V; Kemeny DM. 2014. CD8 T Cells Regulate Allergic Contact Dermatitis by Modulating CCR2-Dependent TNF/iNOS-Expressing Ly6C(+)CD11b(+) Monocytic Cells. J Invest Dermatol 134(3):666-76. [PubMed: 24061165]  [MGI Ref ID J:206039]

Choy JC; Kerjner A; Wong BW; McManus BM; Granville DJ. 2004. Perforin mediates endothelial cell death and resultant transplant vascular disease in cardiac allografts. Am J Pathol 165(1):127-33. [PubMed: 15215168]  [MGI Ref ID J:91236]

Christensen JE; Wodarz D; Christensen JP; Thomsen AR. 2004. Perforin and IFN-gamma do not significantly regulate the virus-specific CD8+ T cell response in the absence of antiviral effector activity. Eur J Immunol 34(5):1389-94. [PubMed: 15114672]  [MGI Ref ID J:89390]

Chrobak P; Gress RE. 2001. Veto activity of activated bone marrow does not require perforin and Fas ligand. Cell Immunol 208(2):80-7. [PubMed: 11333140]  [MGI Ref ID J:127838]

Ciurea A; Hunziker L; Martinic MM; Oxenius A; Hengartner H; Zinkernagel RM. 2001. CD4+ T-cell-epitope escape mutant virus selected in vivo. Nat Med 7(7):795-800. [PubMed: 11433343]  [MGI Ref ID J:134010]

Cretney E; Degli-Esposti MA; Densley EH; Farrell HE; Davis-Poynter NJ; Smyth MJ. 1999. m144, a murine cytomegalovirus (MCMV)-encoded major histocompatibility complex class I homologue, confers tumor resistance to natural killer cell-mediated rejection. J Exp Med 190(3):435-44. [PubMed: 10430631]  [MGI Ref ID J:56787]

Cretney E; Takeda K; Yagita H; Glaccum M; Peschon JJ; Smyth MJ. 2002. Increased susceptibility to tumor initiation and metastasis in TNF-related apoptosis-inducing ligand-deficient mice. J Immunol 168(3):1356-61. [PubMed: 11801676]  [MGI Ref ID J:73948]

Deb C; Lafrance-Corey RG; Schmalstieg WF; Sauer BM; Wang H; German CL; Windebank AJ; Rodriguez M; Howe CL. 2010. CD8+ T cells cause disability and axon loss in a mouse model of multiple sclerosis. PLoS One 5(8):. [PubMed: 20814579]  [MGI Ref ID J:163992]

Deb C; Lafrance-Corey RG; Zoecklein L; Papke L; Rodriguez M; Howe CL. 2009. Demyelinated axons and motor function are protected by genetic deletion of perforin in a mouse model of multiple sclerosis. J Neuropathol Exp Neurol 68(9):1037-48. [PubMed: 19680139]  [MGI Ref ID J:164174]

Decaluwe H; Taillardet M; Corcuff E; Munitic I; Law HK; Rocha B; Riviere Y; Di Santo JP. 2010. {gamma}c deficiency precludes CD8+ T cell memory despite formation of potent T cell effectors. Proc Natl Acad Sci U S A 107(20):9311-6. [PubMed: 20439728]  [MGI Ref ID J:160570]

Deguine J; Breart B; Lemaitre F; Di Santo JP; Bousso P. 2010. Intravital Imaging Reveals Distinct Dynamics for Natural Killer and CD8(+) T Cells during Tumor Regression. Immunity 33(4):632-44. [PubMed: 20951068]  [MGI Ref ID J:165485]

Doloff JC; Waxman DJ. 2012. VEGF receptor inhibitors block the ability of metronomically dosed cyclophosphamide to activate innate immunity-induced tumor regression. Cancer Res 72(5):1103-15. [PubMed: 22237627]  [MGI Ref ID J:181494]

Dudek NL; Thomas HE; Mariana L; Sutherland RM; Allison J; Estella E; Angstetra E; Trapani JA; Santamaria P; Lew AM; Kay TW. 2006. Cytotoxic T-cells from T-cell receptor transgenic NOD8.3 mice destroy beta-cells via the perforin and Fas pathways. Diabetes 55(9):2412-8. [PubMed: 16936188]  [MGI Ref ID J:116592]

Duthie MS; Kahn SJ. 2006. During acute Trypanosoma cruzi infection highly susceptible mice deficient in natural killer cells are protected by a single alpha-galactosylceramide treatment. Immunology 119(3):355-61. [PubMed: 16879622]  [MGI Ref ID J:118525]

Dyer CM; Zhan Y; Brady JL; Carbone FR; Smyth MJ; Lew AM. 2004. Unexpectedly, induction of cytotoxic T lymphocytes enhances the humoral response after DNA immunization. Blood 103(8):3073-5. [PubMed: 15070687]  [MGI Ref ID J:115473]

Ebert G; Preston S; Allison C; Cooney J; Toe JG; Stutz MD; Ojaimi S; Scott HW; Baschuk N; Nachbur U; Torresi J; Chin R; Colledge D; Li X; Warner N; Revill P; Bowden S; Silke J; Begley CG; Pellegrini M. 2015. Cellular inhibitor of apoptosis proteins prevent clearance of hepatitis B virus. Proc Natl Acad Sci U S A 112(18):5797-802. [PubMed: 25902529]  [MGI Ref ID J:221325]

Edinger M; Hoffmann P; Ermann J; Drago K; Fathman CG; Strober S; Negrin RS. 2003. CD4+CD25+ regulatory T cells preserve graft-versus-tumor activity while inhibiting graft-versus-host disease after bone marrow transplantation. Nat Med 9(9):1144-50. [PubMed: 12925844]  [MGI Ref ID J:126172]

Ehl S; Hombach J; Aichele P; Rulicke T; Odermatt B; Hengartner H; Zinkernagel R; Pircher H. 1998. Viral and bacterial infections interfere with peripheral tolerance induction and activate CD8+ T cells to cause immunopathology. J Exp Med 187(5):763-74. [PubMed: 9480986]  [MGI Ref ID J:132027]

Eisenring M; vom Berg J; Kristiansen G; Saller E; Becher B. 2010. IL-12 initiates tumor rejection via lymphoid tissue-inducer cells bearing the natural cytotoxicity receptor NKp46. Nat Immunol 11(11):1030-8. [PubMed: 20935648]  [MGI Ref ID J:166535]

Enomoto N; Hyde E; Ma JZ; Yang J; Forbes-Blom E; Delahunt B; Le Gros G; Ronchese F. 2012. Allergen-specific CTL require perforin expression to suppress allergic airway inflammation. J Immunol 188(4):1734-41. [PubMed: 22250087]  [MGI Ref ID J:181169]

Epardaud M; Elpek KG; Rubinstein MP; Yonekura AR; Bellemare-Pelletier A; Bronson R; Hamerman JA; Goldrath AW; Turley SJ. 2008. Interleukin-15/interleukin-15R alpha complexes promote destruction of established tumors by reviving tumor-resident CD8+ T cells. Cancer Res 68(8):2972-83. [PubMed: 18413767]  [MGI Ref ID J:133960]

Fang R; Ismail N; Walker DH. 2012. Contribution of NK cells to the innate phase of host protection against an intracellular bacterium targeting systemic endothelium. Am J Pathol 181(1):185-95. [PubMed: 22617213]  [MGI Ref ID J:185539]

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Walch M; Dotiwala F; Mulik S; Thiery J; Kirchhausen T; Clayberger C; Krensky AM; Martinvalet D; Lieberman J. 2014. Cytotoxic cells kill intracellular bacteria through granulysin-mediated delivery of granzymes. Cell 157(6):1309-23. [PubMed: 24906149]  [MGI Ref ID J:214451]

Wang Y; Lobigs M; Lee E; Mullbacher A. 2004. Exocytosis and Fas mediated cytolytic mechanisms exert protection from West Nile virus induced encephalitis in mice. Immunol Cell Biol 82(2):170-3. [PubMed: 15061770]  [MGI Ref ID J:90852]

Waring P; Mullbacher A. 2001. Cell death mediated by alloreactive cytotoxic T cells via the granule exocytosis or the Fas pathway is independent of p34cdc2 kinase: Fas dependent killing of cells arrested in the cell cycle. Immunol Cell Biol 79(3):264-73. [PubMed: 11380680]  [MGI Ref ID J:110426]

Weber SE; Tian H; Pirofski LA. 2011. CD8+ cells enhance resistance to pulmonary serotype 3 Streptococcus pneumoniae infection in mice. J Immunol 186(1):432-42. [PubMed: 21135172]  [MGI Ref ID J:168003]

Wei B; Su TT; Dalwadi H; Stephan RP; Fujiwara D; Huang TT; Brewer S; Chen L; Arditi M; Borneman J; Rawlings DJ; Braun J. 2008. Resident enteric microbiota and CD8(+) T cells shape the abundance of marginal zone B cells. Eur J Immunol 38(12):3411-3425. [PubMed: 19009526]  [MGI Ref ID J:141389]

Wei B; Wingender G; Fujiwara D; Chen DY; McPherson M; Brewer S; Borneman J; Kronenberg M; Braun J. 2010. Commensal microbiota and CD8+ T cells shape the formation of invariant NKT cells. J Immunol 184(3):1218-26. [PubMed: 20048124]  [MGI Ref ID J:159495]

Wingender G; Krebs P; Beutler B; Kronenberg M. 2010. Antigen-specific cytotoxicity by invariant NKT cells in vivo is CD95/CD178-dependent and is correlated with antigenic potency. J Immunol 185(5):2721-9. [PubMed: 20660713]  [MGI Ref ID J:163266]

Woodworth JS; Wu Y; Behar SM. 2008. Mycobacterium tuberculosis-specific CD8+ T cells require perforin to kill target cells and provide protection in vivo. J Immunol 181(12):8595-603. [PubMed: 19050279]  [MGI Ref ID J:142057]

Yang J; Huck SP; McHugh RS; Hermans IF; Ronchese F. 2006. Perforin-dependent elimination of dendritic cells regulates the expansion of antigen-specific CD8+ T cells in vivo. Proc Natl Acad Sci U S A 103(1):147-52. [PubMed: 16373503]  [MGI Ref ID J:104557]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

Pricing for USA, Canada and Mexico shipping destinations View International Pricing


Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3435.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing


Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4465.50
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

Control Information

   See control note: Additional control strains are available depending on the researchers needs. Please refer to JAX Notes No. 477 for a complete list of control strains available for NOD/LtJ mice in diabetes research. JAX Notes .
   001976 NOD/ShiLtJ
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

The Jackson Laboratory's Genotype Promise

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.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty


In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.