Strain Name:

C3.129P2(B6)-Il2tm1Hor/J

Stock Number:

002228

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Availability:

Cryopreserved - Ready for recovery

Description

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

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C3H/HeJ
Donor Strain B6;129P-Il2tm1Hor (129P2 derived E14TG2a ES cell line)
 
Donating InvestigatorDr. Ivan Horak,   Forschungs institut fur Molekulare

Appearance
agouti
Related Genotype: A/A

Description
Homozygous mutant mice for the Il2tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the JAX Notes Fall 1996 article.

Control Information

  Control
   Wild-type from the colony
   000659 C3H/HeJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Il2tm1Hor allele
002252   B6.129P2-Il2tm1Hor/J
002229   C.129P2(B6)-Il2tm1Hor/J
002573   NOD.129P2(B6)-Il2tm1Hor/DvsJ
View Strains carrying   Il2tm1Hor     (3 strains)

Strains carrying other alleles of Il2
006102   B10.Cg-H2k Tg(Il2/NFAT-luc)83Rinc/J
006098   B6.Cg-Tg(Il2/NFAT-luc)83Rinc/J
000486   MRL/MpJ
003852   NOD.B6-Il2C57BL/6/Lt
001289   NOD/ShiLt
001976   NOD/ShiLtJ
000686   SJL/J
View Strains carrying other alleles of Il2     (7 strains)

Additional Web Information

JAX® NOTES, Fall 1996; 467. Il2tm1Hor, an Interleukin-2 Gene Targeted Mutation.

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Il2tm1Hor/Il2tm1Hor

        C3.129P2-Il2tm1Hor
  • hematopoietic system phenotype
  • increased CD4-positive T cell number
    • activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion   (MGI Ref ID J:28924)
  • increased CD8-positive T cell number
    • activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin   (MGI Ref ID J:28924)
  • immune system phenotype
  • increased CD4-positive T cell number
    • activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion   (MGI Ref ID J:28924)
  • increased CD8-positive T cell number
    • activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin   (MGI Ref ID J:28924)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Il2tm1Hor/Il2tm1Hor

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • premature death
    • about of 50% of mice die within the first 9 weeks of age with enlarged lymphoid organs and severe anemia   (MGI Ref ID J:15223)
    • the remaining mice die by 25 weeks of age from inflammatory bowel disease   (MGI Ref ID J:15223)
  • digestive/alimentary phenotype
  • abnormal intestinal epithelium morphology
    • prominent epithelial regeneration with crypt branching and dysplasia near areas of inflammation   (MGI Ref ID J:15223)
    • crypt hyperplasia and unusual branching is observed   (MGI Ref ID J:29999)
    • abnormal intestinal goblet cell morphology
      • colon epithelium shows loss of goblet cells   (MGI Ref ID J:15223)
      • loss of mucin is observed in goblet cells   (MGI Ref ID J:29999)
    • crypts of Lieberkuhn abscesses
      • frequently occurres in the large intestine   (MGI Ref ID J:15223)
    • intestinal ulcer
      • ulcers occur in the large intestine, with pronounced thickening of the bowel wall   (MGI Ref ID J:15223)
  • colitis
    • all mice that do not die within the first 9 weeks after birth develop an inflammatory bowel disease that is similar to the human disease ulcerative colitis   (MGI Ref ID J:15223)
    • infiltrating lymphocytes sometimes form nodules   (MGI Ref ID J:15223)
    • mice bred in a germ-free facility do not display any histopathological signs of colitis   (MGI Ref ID J:15223)
    • mice bred under specific pathogen free conditions do not develop any clinical signs of colitis but histological and immunological examinations show the beginning of inflammatory processes in mice that are 17-20 weeks of age   (MGI Ref ID J:15223)
    • occurs in all mice that survive past 9 weeks of age, with thickening of large intestinal wall   (MGI Ref ID J:29999)
    • mice kept under a specific pathogen free environment develop colitis when immunized with an antigen that activates CD4 T cells   (MGI Ref ID J:37220)
  • diarrhea
    • occurs in mice 24 weeks of age   (MGI Ref ID J:29999)
    • chronic diarrhea
      • all mice that do not die within the first 9 weeks after birth exhibit diarrhea   (MGI Ref ID J:15223)
  • rectal hemorrhage
    • rarely observed   (MGI Ref ID J:29999)
  • rectal prolapse
    • occasional occurrence among mice whom live past 9 weeks of age   (MGI Ref ID J:29999)
    • frequent occurrence among mice whom live past 9 weeks of age   (MGI Ref ID J:15223)
  • immune system phenotype
  • abnormal immune system organ morphology
    • proliferative response of splenocytes to anti-CD3 antibody is only 16% of wt controls   (MGI Ref ID J:79241)
    • poor proliferative response to anti-CD3 antibody is partially rescued by addition of cytokines including IL-2, IL-4, IL-7   (MGI Ref ID J:79241)
    • there is reduced proliferation to allogenic leukocytes   (MGI Ref ID J:79241)
    • enlarged lymph nodes   (MGI Ref ID J:15223)
      • lymph node hyperplasia   (MGI Ref ID J:16662)
    • enlarged mesenteric lymph nodes
      • increased 3-10 fold in size as compared to control littermates   (MGI Ref ID J:29999)
    • enlarged spleen
      • occurs in the 50% of mice that die prematurely   (MGI Ref ID J:15223)
  • abnormal lymphocyte morphology
    • decreased apoptosis in thymus upon injection with anti-CD3 antibody   (MGI Ref ID J:37220)
    • abnormal CD8 positive, alpha-beta intraepithelial T cell morphology
      • increased number (5-100 fold) are found in diseased colon   (MGI Ref ID J:15223)
      • T cells expressing the CD8 alpha-beta heterodimer predominate over CD8 alpha-alpha T cells   (MGI Ref ID J:39981)
    • abnormal T-helper 1 cell differentiation
      • 10 fold greater amounts of IFN gamma were made by thymocytes from immunized mutant mice as measured by an in vitro assay   (MGI Ref ID J:37220)
      • low levels of the Th2 cytokine IL-4 were made compared to the large level made by wt thymocytes   (MGI Ref ID J:37220)
      • however, treatment with an IL-12 neutralizing antibody normalized Th1cytokine levels   (MGI Ref ID J:37220)
    • abnormal class switch recombination
      • there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus   (MGI Ref ID J:15573)
    • abnormal gamma-delta intraepithelial T cell morphology
      • decreased percentage of these cells are found in the colon epithelium   (MGI Ref ID J:15223)
    • abnormal lymphocyte cell number   (MGI Ref ID J:15223)
      • decreased double-negative T cell number
        • there is a drastic reduction in the colon   (MGI Ref ID J:15223)
      • decreased double-positive T cell number
        • percentage of these cells is decreased (47.0% vs 86.2%) in the thymus when mice are immunized with a CD4 T cell activating antigen   (MGI Ref ID J:37220)
      • increased double-negative T cell number
        • percentage of these cells is increased (11.2% vs 3.7%) in the thymus when mice are immunized with a CD4 T cell activating antigen   (MGI Ref ID J:37220)
      • increased pre-B cell number
        • of cells in the bone marrow   (MGI Ref ID J:16662)
      • increased single-positive T cell number
        • percentage of these cells is increased (41.8% vs 20.9.2%) in the thymus when mice are immunized with a CD4 T cell activating antigen   (MGI Ref ID J:37220)
        • however, treatment with an IL-12 neutralizing antibody normalized SP cell numbers   (MGI Ref ID J:37220)
    • abnormal thymocyte activation
      • increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1   (MGI Ref ID J:37220)
      • however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes   (MGI Ref ID J:37220)
      • in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody   (MGI Ref ID J:39989)
    • decreased T cell proliferation   (MGI Ref ID J:26198)
    • increased B cell proliferation
      • B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate   (MGI Ref ID J:16662)
    • increased T cell proliferation
      • the proliferation of T cells in the colon is twice that of wild-type controls   (MGI Ref ID J:15223)
      • 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate   (MGI Ref ID J:16662)
    • increased pro-B cell number
      • of cells in the bone marrow   (MGI Ref ID J:16662)
  • abnormal lymphocyte physiology   (MGI Ref ID J:15223)
    • abnormal CD4-positive T cell physiology
      • there is an impaired ability to induce Ig class switching in B cells after infection with vesicular stomatitis virus   (MGI Ref ID J:15573)
      • increased cytotoxic effectiveness of CD4 T cells isolated from the colon   (MGI Ref ID J:39981)
      • unable to induce IgM secretion from activated B cells in an in vitro assay   (MGI Ref ID J:39989)
      • however, IgM levels are in vivo are normal   (MGI Ref ID J:39989)
    • abnormal class switch recombination
      • there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus   (MGI Ref ID J:15573)
    • abnormal cytotoxic T cell physiology
      • enhanced target cell killing by intraepithelial lymphocytes T cells (IEL) and lamina propia lymphocytes of the large intestine   (MGI Ref ID J:39981)
      • enhanced target cell killing by intraepithelial lymphocytes T cells (IEL) of the small intestine   (MGI Ref ID J:39981)
      • defective cytotoxic T cell cytolysis
        • there is a three fold reduction of target cell killing by primary T cells in a chromium release assay   (MGI Ref ID J:15573)
        • no target cell killing by previously stimulated T cells in a chromium release assay   (MGI Ref ID J:15573)
        • there is reduced killing of allogeneic tumor cells in an in vitro assay   (MGI Ref ID J:26198)
        • footpad swelling is reduced 6-10 days after infection with lymphocytic choriomeningitis virus   (MGI Ref ID J:26861)
    • abnormal level of surface class II molecules
      • expression occurs in high number of colon epithelial cells   (MGI Ref ID J:15223)
    • abnormal thymocyte activation
      • increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1   (MGI Ref ID J:37220)
      • however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes   (MGI Ref ID J:37220)
      • in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody   (MGI Ref ID J:39989)
    • decreased T cell proliferation   (MGI Ref ID J:26198)
    • impaired natural killer cell mediated cytotoxicity
      • 3 to 9 fold reduction in killing of NK susceptible target cells as measured by chromium release assay   (MGI Ref ID J:15573)
    • increased B cell proliferation
      • B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate   (MGI Ref ID J:16662)
    • increased IgA level
      • drastic elevation in secretion by B cells found in the colon   (MGI Ref ID J:15223)
    • increased IgE level
      • levels are 10 fold higher than those observed in wild-type mice   (MGI Ref ID J:16662)
    • increased IgG1 level
      • drastic elevation in secretion of IgG1 by B cells found in the colon   (MGI Ref ID J:15223)
      • levels of IgG1 are increased 100 fold   (MGI Ref ID J:16662)
      • levels of IgG1 are drastically increased to levels above 2700 ug/ml   (MGI Ref ID J:39989)
    • increased IgG2a level
      • levels of IgG2a are also elevated   (MGI Ref ID J:16662)
    • increased IgG2b level
      • levels of IgG2b are also elevated   (MGI Ref ID J:16662)
    • increased T cell proliferation
      • the proliferation of T cells in the colon is twice that of wild-type controls   (MGI Ref ID J:15223)
      • 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate   (MGI Ref ID J:16662)
  • colitis
    • all mice that do not die within the first 9 weeks after birth develop an inflammatory bowel disease that is similar to the human disease ulcerative colitis   (MGI Ref ID J:15223)
    • infiltrating lymphocytes sometimes form nodules   (MGI Ref ID J:15223)
    • mice bred in a germ-free facility do not display any histopathological signs of colitis   (MGI Ref ID J:15223)
    • mice bred under specific pathogen free conditions do not develop any clinical signs of colitis but histological and immunological examinations show the beginning of inflammatory processes in mice that are 17-20 weeks of age   (MGI Ref ID J:15223)
    • occurs in all mice that survive past 9 weeks of age, with thickening of large intestinal wall   (MGI Ref ID J:29999)
    • mice kept under a specific pathogen free environment develop colitis when immunized with an antigen that activates CD4 T cells   (MGI Ref ID J:37220)
  • increased length of allograft survival
    • graft rejection of allogeneic pancreatic islet cells is delayed by 11 days compared to controls   (MGI Ref ID J:26198)
  • increased susceptibility to viral infection
    • despite reduced cytotoxic T cell activity, mice still clear lymphocytic choriomeningitis virus within nine days of infection   (MGI Ref ID J:26861)
  • growth/size/body phenotype
  • cachexia
    • weight loss resulting from intestinal inflammation is observed by 24 weeks   (MGI Ref ID J:29999)
  • hematopoietic system phenotype
  • abnormal lymphocyte morphology
    • decreased apoptosis in thymus upon injection with anti-CD3 antibody   (MGI Ref ID J:37220)
    • abnormal CD8 positive, alpha-beta intraepithelial T cell morphology
      • increased number (5-100 fold) are found in diseased colon   (MGI Ref ID J:15223)
      • T cells expressing the CD8 alpha-beta heterodimer predominate over CD8 alpha-alpha T cells   (MGI Ref ID J:39981)
    • abnormal T-helper 1 cell differentiation
      • 10 fold greater amounts of IFN gamma were made by thymocytes from immunized mutant mice as measured by an in vitro assay   (MGI Ref ID J:37220)
      • low levels of the Th2 cytokine IL-4 were made compared to the large level made by wt thymocytes   (MGI Ref ID J:37220)
      • however, treatment with an IL-12 neutralizing antibody normalized Th1cytokine levels   (MGI Ref ID J:37220)
    • abnormal class switch recombination
      • there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus   (MGI Ref ID J:15573)
    • abnormal gamma-delta intraepithelial T cell morphology
      • decreased percentage of these cells are found in the colon epithelium   (MGI Ref ID J:15223)
    • abnormal lymphocyte cell number   (MGI Ref ID J:15223)
      • decreased double-negative T cell number
        • there is a drastic reduction in the colon   (MGI Ref ID J:15223)
      • decreased double-positive T cell number
        • percentage of these cells is decreased (47.0% vs 86.2%) in the thymus when mice are immunized with a CD4 T cell activating antigen   (MGI Ref ID J:37220)
      • increased double-negative T cell number
        • percentage of these cells is increased (11.2% vs 3.7%) in the thymus when mice are immunized with a CD4 T cell activating antigen   (MGI Ref ID J:37220)
      • increased pre-B cell number
        • of cells in the bone marrow   (MGI Ref ID J:16662)
      • increased single-positive T cell number
        • percentage of these cells is increased (41.8% vs 20.9.2%) in the thymus when mice are immunized with a CD4 T cell activating antigen   (MGI Ref ID J:37220)
        • however, treatment with an IL-12 neutralizing antibody normalized SP cell numbers   (MGI Ref ID J:37220)
    • abnormal thymocyte activation
      • increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1   (MGI Ref ID J:37220)
      • however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes   (MGI Ref ID J:37220)
      • in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody   (MGI Ref ID J:39989)
    • decreased T cell proliferation   (MGI Ref ID J:26198)
    • increased B cell proliferation
      • B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate   (MGI Ref ID J:16662)
    • increased T cell proliferation
      • the proliferation of T cells in the colon is twice that of wild-type controls   (MGI Ref ID J:15223)
      • 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate   (MGI Ref ID J:16662)
    • increased pro-B cell number
      • of cells in the bone marrow   (MGI Ref ID J:16662)
  • abnormal lymphocyte physiology   (MGI Ref ID J:15223)
    • abnormal CD4-positive T cell physiology
      • there is an impaired ability to induce Ig class switching in B cells after infection with vesicular stomatitis virus   (MGI Ref ID J:15573)
      • increased cytotoxic effectiveness of CD4 T cells isolated from the colon   (MGI Ref ID J:39981)
      • unable to induce IgM secretion from activated B cells in an in vitro assay   (MGI Ref ID J:39989)
      • however, IgM levels are in vivo are normal   (MGI Ref ID J:39989)
    • abnormal class switch recombination
      • there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus   (MGI Ref ID J:15573)
    • abnormal cytotoxic T cell physiology
      • enhanced target cell killing by intraepithelial lymphocytes T cells (IEL) and lamina propia lymphocytes of the large intestine   (MGI Ref ID J:39981)
      • enhanced target cell killing by intraepithelial lymphocytes T cells (IEL) of the small intestine   (MGI Ref ID J:39981)
      • defective cytotoxic T cell cytolysis
        • there is a three fold reduction of target cell killing by primary T cells in a chromium release assay   (MGI Ref ID J:15573)
        • no target cell killing by previously stimulated T cells in a chromium release assay   (MGI Ref ID J:15573)
        • there is reduced killing of allogeneic tumor cells in an in vitro assay   (MGI Ref ID J:26198)
        • footpad swelling is reduced 6-10 days after infection with lymphocytic choriomeningitis virus   (MGI Ref ID J:26861)
    • abnormal level of surface class II molecules
      • expression occurs in high number of colon epithelial cells   (MGI Ref ID J:15223)
    • abnormal thymocyte activation
      • increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1   (MGI Ref ID J:37220)
      • however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes   (MGI Ref ID J:37220)
      • in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody   (MGI Ref ID J:39989)
    • decreased T cell proliferation   (MGI Ref ID J:26198)
    • impaired natural killer cell mediated cytotoxicity
      • 3 to 9 fold reduction in killing of NK susceptible target cells as measured by chromium release assay   (MGI Ref ID J:15573)
    • increased B cell proliferation
      • B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate   (MGI Ref ID J:16662)
    • increased IgA level
      • drastic elevation in secretion by B cells found in the colon   (MGI Ref ID J:15223)
    • increased IgE level
      • levels are 10 fold higher than those observed in wild-type mice   (MGI Ref ID J:16662)
    • increased IgG1 level
      • drastic elevation in secretion of IgG1 by B cells found in the colon   (MGI Ref ID J:15223)
      • levels of IgG1 are increased 100 fold   (MGI Ref ID J:16662)
      • levels of IgG1 are drastically increased to levels above 2700 ug/ml   (MGI Ref ID J:39989)
    • increased IgG2a level
      • levels of IgG2a are also elevated   (MGI Ref ID J:16662)
    • increased IgG2b level
      • levels of IgG2b are also elevated   (MGI Ref ID J:16662)
    • increased T cell proliferation
      • the proliferation of T cells in the colon is twice that of wild-type controls   (MGI Ref ID J:15223)
      • 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate   (MGI Ref ID J:16662)
  • anemia
    • severe anemia is found in 50% of mice that die prematurely   (MGI Ref ID J:15223)
    • occurs in mice 24 weeks of age   (MGI Ref ID J:29999)
  • enlarged spleen
    • occurs in the 50% of mice that die prematurely   (MGI Ref ID J:15223)
  • endocrine/exocrine gland phenotype
  • abnormal thymocyte activation
    • increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1   (MGI Ref ID J:37220)
    • however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes   (MGI Ref ID J:37220)
    • in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody   (MGI Ref ID J:39989)
  • crypts of Lieberkuhn abscesses
    • frequently occurres in the large intestine   (MGI Ref ID J:15223)
  • behavior/neurological phenotype
  • hunched posture
    • occurs in mice 24 weeks of age   (MGI Ref ID J:29999)
  • cardiovascular system phenotype
  • rectal hemorrhage
    • rarely observed   (MGI Ref ID J:29999)
  • homeostasis/metabolism phenotype
  • amyloidosis
    • predominately in liver, spleen, and kidneys   (MGI Ref ID J:15223)

Il2tm1Hor/Il2tm1Hor

        C.129P2-Il2tm1Hor
  • mortality/aging
  • premature death
    • mice all die by 5 weeks of age, compared to death by 25 weeks of age for mice homozygous for the same mutant locus on a B6.129P2 background mice all die by 5 weeks of age, compared to death by 25 weeks of age for mice with the same mutant locus on a mixed genetic background   (MGI Ref ID J:29799)
  • immune system phenotype
  • abnormal lymphocyte morphology   (MGI Ref ID J:29799)
    • increased B cell proliferation
      • faster proliferation as measured by BrdU incorporation   (MGI Ref ID J:29799)
    • increased T cell proliferation
      • by 10 days of age, T cells in lymph nodes express high levels of activation markers and are proliferating at an increased rate   (MGI Ref ID J:29799)
      • CD4 T cells are activated prior to CD8 T cells (10 days vs. 15 days of age)   (MGI Ref ID J:29799)
    • increased germinal center B cell number   (MGI Ref ID J:29799)
    • increased plasma cell number
      • seen in the spleen by 15 days of age   (MGI Ref ID J:29799)
  • abnormal regulatory T cell physiology
    • there is a rapid loss of adoptively transferred regulatory T cells   (MGI Ref ID J:112603)
  • abnormal spleen morphology   (MGI Ref ID J:29799)
    • increased spleen red pulp amount   (MGI Ref ID J:29799)
    • spleen hyperplasia
      • 15 day old mice exhibit hyperplasia of the white pulp   (MGI Ref ID J:29799)
  • enlarged lymph nodes   (MGI Ref ID J:29799)
  • increased IgG level
    • increased level of IgG secreting B cells from spleen and lymph nodes   (MGI Ref ID J:29799)
  • increased inflammatory response   (MGI Ref ID J:29799)
    • heart inflammation
      • moderate to severe inflammation noted upon necropsy   (MGI Ref ID J:29799)
    • liver inflammation   (MGI Ref ID J:29799)
    • lung inflammation
      • moderate to severe inflammation noted upon necropsy   (MGI Ref ID J:29799)
    • pancreas inflammation
      • moderate to severe inflammation noted upon necropsy   (MGI Ref ID J:29799)
    • vasculitis
      • moderate to severe inflammation noted in the major thoracic blood vessels upon necropsy   (MGI Ref ID J:29799)
  • increased susceptibility to autoimmune hemolytic anemia
    • cause of death for mice on this genetic background, as opposed to death caused by inflammatory bowel disease for homozygous mice on a B6.129P2 genetic background   (MGI Ref ID J:29799)
  • hematopoietic system phenotype
  • abnormal bone marrow cell number
    • invasion of T cells occur, with a concurrent drop in B cells and other nucleated cells   (MGI Ref ID J:29799)
  • abnormal lymphocyte morphology   (MGI Ref ID J:29799)
    • increased B cell proliferation
      • faster proliferation as measured by BrdU incorporation   (MGI Ref ID J:29799)
    • increased T cell proliferation
      • by 10 days of age, T cells in lymph nodes express high levels of activation markers and are proliferating at an increased rate   (MGI Ref ID J:29799)
      • CD4 T cells are activated prior to CD8 T cells (10 days vs. 15 days of age)   (MGI Ref ID J:29799)
    • increased germinal center B cell number   (MGI Ref ID J:29799)
    • increased plasma cell number
      • seen in the spleen by 15 days of age   (MGI Ref ID J:29799)
  • abnormal regulatory T cell physiology
    • there is a rapid loss of adoptively transferred regulatory T cells   (MGI Ref ID J:112603)
  • abnormal reticulocyte morphology
    • marked reduction concurrent with T cell invasion of marrow   (MGI Ref ID J:29799)
  • abnormal spleen morphology   (MGI Ref ID J:29799)
    • increased spleen red pulp amount   (MGI Ref ID J:29799)
    • spleen hyperplasia
      • 15 day old mice exhibit hyperplasia of the white pulp   (MGI Ref ID J:29799)
  • decreased hematocrit   (MGI Ref ID J:29799)
  • increased IgG level
    • increased level of IgG secreting B cells from spleen and lymph nodes   (MGI Ref ID J:29799)
  • increased mean corpuscular hemoglobin
    • about twice normal levels, this indicates a hyperchromic anemia   (MGI Ref ID J:29799)
  • increased susceptibility to autoimmune hemolytic anemia
    • cause of death for mice on this genetic background, as opposed to death caused by inflammatory bowel disease for homozygous mice on a B6.129P2 genetic background   (MGI Ref ID J:29799)
  • low mean erythrocyte cell number   (MGI Ref ID J:29799)
  • homeostasis/metabolism phenotype
  • increased circulating bilirubin level   (MGI Ref ID J:29799)
  • cardiovascular system phenotype
  • heart inflammation
    • moderate to severe inflammation noted upon necropsy   (MGI Ref ID J:29799)
  • vasculitis
    • moderate to severe inflammation noted in the major thoracic blood vessels upon necropsy   (MGI Ref ID J:29799)
  • endocrine/exocrine gland phenotype
  • pancreas inflammation
    • moderate to severe inflammation noted upon necropsy   (MGI Ref ID J:29799)
  • liver/biliary system phenotype
  • liver inflammation   (MGI Ref ID J:29799)
  • respiratory system phenotype
  • lung inflammation
    • moderate to severe inflammation noted upon necropsy   (MGI Ref ID J:29799)

Il2tm1Hor/Il2tm1Hor

        B6.129P2-Il2tm1Hor
  • immune system phenotype
  • *normal* immune system phenotype
    • bone marrow chimeras (mutant bone marrow in Rag2-deficient hosts) do not develop a wasting autoimmune disease compared to the lethal disease that develops with Il2ratm1Dw bone marrow chimeras   (MGI Ref ID J:125748)
    • increased T cell number   (MGI Ref ID J:125748)
      • increased CD4-positive T cell number
        • activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion   (MGI Ref ID J:28924)
      • increased CD8-positive T cell number
        • activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin   (MGI Ref ID J:28924)
      • increased activated T cell number
        • higher numbers due to less sensitivity to Fas-mediated cell death (apoptosis)   (MGI Ref ID J:28924)
    • increased T cell proliferation
      • T cells continue to respond to antigen instead of going into anergy during secondary stimulation with antigens   (MGI Ref ID J:28924)
  • hematopoietic system phenotype
  • increased T cell number   (MGI Ref ID J:125748)
    • increased CD4-positive T cell number
      • activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion   (MGI Ref ID J:28924)
    • increased CD8-positive T cell number
      • activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin   (MGI Ref ID J:28924)
    • increased activated T cell number
      • higher numbers due to less sensitivity to Fas-mediated cell death (apoptosis)   (MGI Ref ID J:28924)
  • increased T cell proliferation
    • T cells continue to respond to antigen instead of going into anergy during secondary stimulation with antigens   (MGI Ref ID J:28924)

Il2tm1Hor/Il2tm1Hor

        B6.129P2-Il2tm1Hor/J
  • immune system phenotype
  • abnormal T cell activation
    • both CD4+ and CD8+ T cells fail to increase in size and granularity after activation with anti-CD3/28   (MGI Ref ID J:190168)
    • abnormal T cell proliferation
      • DNA replication fails to increase in activated CD4+ and CD8+ T cells after activation with anti-CD3/28   (MGI Ref ID J:190168)
  • abnormal circulating cytokine level   (MGI Ref ID J:190168)
    • decreased circulating interferon-gamma level
      • after activation with anti-CD3/28   (MGI Ref ID J:190168)
    • decreased circulating interleukin-13 level
      • after activation with anti-CD3/28   (MGI Ref ID J:190168)
    • decreased circulating interleukin-4 level
      • after activation with anti-CD3/28   (MGI Ref ID J:190168)
  • abnormal response to transplant
    • wild-type regulatory T cells fail to engraft when adoptively transferred into these mice   (MGI Ref ID J:113547)
  • decreased regulatory T cell number
    • there is a 2 to 5 fold reduction in the percentage of CD25-postive CD4 T cells in both the thymus and lymph nodes   (MGI Ref ID J:113547)
    • decreased CD4-positive, CD25-positive, alpha-beta regulatory T cell number
  • enlarged lymph nodes
    • increased cellularity of lymph nodes compared to wild-type mice, but lower than what is observed in Il2rbtm1Mak mice   (MGI Ref ID J:113547)
  • increased CD4-positive T cell number
  • increased splenocyte number   (MGI Ref ID J:131774)
  • increased susceptibility to autoimmune disorder
    • generalized symptoms of autoimmunity noted at 4 weeks of age   (MGI Ref ID J:113547)
    • transfer of wild-type regulatory T cells did not prevent autoimmune disorder   (MGI Ref ID J:113547)
  • cellular phenotype
  • abnormal cellular respiration
    • fail to switch from oxidative phosphorylation to aerobic glycolysis after 5 days of tamoxifen treatment and activation with anti-CD3/28   (MGI Ref ID J:190168)
  • homeostasis/metabolism phenotype
  • abnormal circulating cytokine level   (MGI Ref ID J:190168)
    • decreased circulating interferon-gamma level
      • after activation with anti-CD3/28   (MGI Ref ID J:190168)
    • decreased circulating interleukin-13 level
      • after activation with anti-CD3/28   (MGI Ref ID J:190168)
    • decreased circulating interleukin-4 level
      • after activation with anti-CD3/28   (MGI Ref ID J:190168)
  • hematopoietic system phenotype
  • abnormal T cell activation
    • both CD4+ and CD8+ T cells fail to increase in size and granularity after activation with anti-CD3/28   (MGI Ref ID J:190168)
    • abnormal T cell proliferation
      • DNA replication fails to increase in activated CD4+ and CD8+ T cells after activation with anti-CD3/28   (MGI Ref ID J:190168)
  • decreased regulatory T cell number
    • there is a 2 to 5 fold reduction in the percentage of CD25-postive CD4 T cells in both the thymus and lymph nodes   (MGI Ref ID J:113547)
    • decreased CD4-positive, CD25-positive, alpha-beta regulatory T cell number
  • increased CD4-positive T cell number
  • increased splenocyte number   (MGI Ref ID J:131774)

Il2tm1Hor/Il2tm1Hor

        involves: 129P2/OlaHsd
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • there are no abnormalities of the placenta, the mesometrial triangle, and differentiation of granulated metrial gland cells (aka uterine NK cells) in the uteri of pregnant mice at day 14 of gestation   (MGI Ref ID J:134589)
  • immune system phenotype
  • increased regulatory T cell number
    • of CD25lo regulatory T cells   (MGI Ref ID J:208318)
  • hematopoietic system phenotype
  • increased regulatory T cell number
    • of CD25lo regulatory T cells   (MGI Ref ID J:208318)

Il2tm1Hor/Il2tm1Hor

        involves: 129P2/OlaHsd * C57BL/6J
  • immune system phenotype
  • increased T-helper 17 cell number
    • increase in the percentage of IL-17-producing cells in culturing CD4+ T cells in vitro under Th17-polarizing conditions   (MGI Ref ID J:120176)
    • greater proportion of IL-17-positive cells (most of which CD4 positive) in peripheral lymph nodes   (MGI Ref ID J:120176)
    • 30-fold difference in absolute numbers of mesenteric Th17 cells compared with wild-type mice   (MGI Ref ID J:120176)
  • increased circulating interleukin-17 level
    • elevated serum IL-17 concentration at 3 months old   (MGI Ref ID J:120176)
  • homeostasis/metabolism phenotype
  • increased circulating interleukin-17 level
    • elevated serum IL-17 concentration at 3 months old   (MGI Ref ID J:120176)
  • hematopoietic system phenotype
  • increased T-helper 17 cell number
    • increase in the percentage of IL-17-producing cells in culturing CD4+ T cells in vitro under Th17-polarizing conditions   (MGI Ref ID J:120176)
    • greater proportion of IL-17-positive cells (most of which CD4 positive) in peripheral lymph nodes   (MGI Ref ID J:120176)
    • 30-fold difference in absolute numbers of mesenteric Th17 cells compared with wild-type mice   (MGI Ref ID J:120176)
View Research Applications

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

Immunology, Inflammation and Autoimmunity Research
Inflammation
      Inflammatory bowel disease

Il2tm1Hor related

Cancer Research
Growth Factors/Receptors/Cytokines

Hematological Research
Anemia, Iron Deficiency and Transport Defects
      hemolytic
Immunological Defects

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
      hemolytic anemia
Growth Factors/Receptors/Cytokines

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Il2tm1Hor
Allele Name targeted mutation 1, Ivan Horak
Allele Type Targeted (Null/Knockout)
Common Name(s) IL-2 KO; IL-2-; IL-2null; Il2-;
Mutation Made ByDr. Ivan Horak,   Forschungs institut fur Molekulare
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Il2, interleukin 2
Chromosome 3
Gene Common Name(s) IL-2; Il-2; TCGF; lymphokine;
General Note Phenotypic Similarity to Human Syndrome: Inflammatory Bowel Disease (J:15223).Phenotypic Similarity to Human Syndrome: Inflammatory Bowel Disease (J:51450) with B2m.
Molecular Note Insertion of a neomycin-resistance gene into the third exon introduced several stop codons in all reading frames. [MGI Ref ID J:39989]

Genotyping

Genotyping Information

Genotyping Protocols

Il2tm1Hor, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Schorle H; Holtschke T; Hunig T; Schimpl A; Horak I. 1991. Development and function of T cells in mice rendered interleukin-2 deficient by gene targeting. Nature 352(6336):621-4. [PubMed: 1830926]  [MGI Ref ID J:39989]

Additional References

Antony PA; Paulos CM; Ahmadzadeh M; Akpinarli A; Palmer DC; Sato N; Kaiser A; Hinrichs CS; Klebanoff CA; Tagaya Y; Restifo NP. 2006. Interleukin-2-dependent mechanisms of tolerance and immunity in vivo. J Immunol 176(9):5255-66. [PubMed: 16621991]  [MGI Ref ID J:115150]

Horak I. 1995. Immunodeficiency in IL-2-knockout mice. Clin Immunol Immunopathol 76(3 Pt 2):S172-3. [PubMed: 7554463]  [MGI Ref ID J:28804]

Kundig TM; Schorle H; Bachmann MF; Hengartner H; Zinkernagel RM; Horak I. 1993. Immune responses in interleukin-2-deficient mice. Science 262(5136):1059-61. [PubMed: 8235625]  [MGI Ref ID J:15573]

Sadlack B; Lohler J; Schorle H; Klebb G; Haber H; Sickel E; Noelle RJ; Horak I. 1995. Generalized autoimmune disease in interleukin-2-deficient mice is triggered by an uncontrolled activation and proliferation of CD4+ T cells. Eur J Immunol 25(11):3053-9. [PubMed: 7489743]  [MGI Ref ID J:29799]

Sadlack B; Merz H; Schorle H; Schimpl A; Feller AC; Horak I. 1993. Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene [see comments] Cell 75(2):253-61. [PubMed: 8402910]  [MGI Ref ID J:15223]

Il2tm1Hor related

Almeida AR; Legrand N; Papiernik M; Freitas AA. 2002. Homeostasis of peripheral CD4+ T cells: IL-2R alpha and IL-2 shape a population of regulatory cells that controls CD4+ T cell numbers. J Immunol 169(9):4850-60. [PubMed: 12391195]  [MGI Ref ID J:125748]

Antony PA; Paulos CM; Ahmadzadeh M; Akpinarli A; Palmer DC; Sato N; Kaiser A; Hinrichs CS; Klebanoff CA; Tagaya Y; Restifo NP. 2006. Interleukin-2-dependent mechanisms of tolerance and immunity in vivo. J Immunol 176(9):5255-66. [PubMed: 16621991]  [MGI Ref ID J:115150]

Antony PA; Piccirillo CA; Akpinarli A; Finkelstein SE; Speiss PJ; Surman DR; Palmer DC; Chan CC; Klebanoff CA; Overwijk WW; Rosenberg SA; Restifo NP. 2005. CD8+ T cell immunity against a tumor/self-antigen is augmented by CD4+ T helper cells and hindered by naturally occurring T regulatory cells. J Immunol 174(5):2591-601. [PubMed: 15728465]  [MGI Ref ID J:129825]

Antov A; Yang L; Vig M; Baltimore D; Van Parijs L. 2003. Essential role for STAT5 signaling in CD25+CD4+ regulatory T cell homeostasis and the maintenance of self-tolerance. J Immunol 171(7):3435-41. [PubMed: 14500638]  [MGI Ref ID J:85631]

Ashcroft AJ; Cruickshank SM; Croucher PI; Perry MJ; Rollinson S; Lippitt JM; Child JA; Dunstan C; Felsburg PJ; Morgan GJ; Carding SR. 2003. Colonic dendritic cells, intestinal inflammation, and T cell-mediated bone destruction are modulated by recombinant osteoprotegerin. Immunity 19(6):849-61. [PubMed: 14670302]  [MGI Ref ID J:86997]

Bachmann MF; Schorle H; Kuhn R; Muller W; Hengartner H; Zinkernagel RM; Horak I. 1995. Antiviral immune responses in mice deficient for both interleukin-2 and interleukin-4. J Virol 69(8):4842-6. [PubMed: 7609051]  [MGI Ref ID J:26861]

Barmeyer C; Harren M; Schmitz H; Heinzel-Pleines U; Mankertz J; Seidler U; Horak I; Wiedenmann B; Fromm M; Schulzke JD. 2004. Mechanisms of diarrhea in the interleukin-2-deficient mouse model of colonic inflammation. Am J Physiol Gastrointest Liver Physiol 286(2):G244-52. [PubMed: 14715519]  [MGI Ref ID J:87603]

Barmeyer C; Horak I; Zeitz M; Fromm M; Schulzke JD. 2002. The interleukin-2-deficient mouse model Pathobiology 70(3):139-42. [PubMed: 12571417]  [MGI Ref ID J:82223]

Bassiri H; Carding SR. 2001. A requirement for IL-2/IL-2 receptor signaling in intrathymic negative selection. J Immunol 166(10):5945-54. [PubMed: 11342609]  [MGI Ref ID J:110891]

Batchelder JM; Burns JM Jr; Cigel FK; Lieberg H; Manning DD; Pepper BJ; Yanez DM; van der Heyde H; Weidanz WP. 2003. Plasmodium chabaudi adami: interferon-gamma but not IL-2 is essential for the expression of cell-mediated immunity against blood-stage parasites in mice. Exp Parasitol 105(2):159-66. [PubMed: 14969693]  [MGI Ref ID J:102606]

Bayer AL; Chirinos J; Cabello C; Yang J; Matsutani T; Malek TR; Levy RB. 2011. Expansion of a restricted residual host T reg-cell repertoire is dependent on IL-2 following experimental autologous hematopoietic stem transplantation. Eur J Immunol 41(12):3467-78. [PubMed: 21928285]  [MGI Ref ID J:179509]

Beck RD Jr; King MA; Ha GK; Cushman JD; Huang Z; Petitto JM. 2005. IL-2 deficiency results in altered septal and hippocampal cytoarchitecture: relation to development and neurotrophins. J Neuroimmunol 160(1-2):146-53. [PubMed: 15710467]  [MGI Ref ID J:101962]

Beck RD Jr; Wasserfall C; Ha GK; Cushman JD; Huang Z; Atkinson MA; Petitto JM. 2005. Changes in hippocampal IL-15, related cytokines, and neurogenesis in IL-2 deficient mice. Brain Res 1041(2):223-230. [PubMed: 15829231]  [MGI Ref ID J:97426]

Beck RD; King MA; Huang Z; Petitto JM. 2002. Alterations in septohippocampal cholinergic neurons resulting from interleukin-2 gene knockout. Brain Res 955(1-2):16-23. [PubMed: 12419517]  [MGI Ref ID J:80486]

Behrens GM; Li M; Davey GM; Allison J; Flavell RA; Carbone FR; Heath WR. 2004. Helper requirements for generation of effector CTL to islet beta cell antigens. J Immunol 172(9):5420-6. [PubMed: 15100283]  [MGI Ref ID J:89639]

Bemiss CJ; Mahon BD; Henry A; Weaver V; Cantorna MT. 2002. Interleukin-2 is one of the targets of 1,25-dihydroxyvitamin D3 in the immune system. Arch Biochem Biophys 402(2):249-54. [PubMed: 12051670]  [MGI Ref ID J:114521]

Beyersdorf N; Ding X; Tietze JK; Hanke T. 2007. Characterization of mouse CD4 T cell subsets defined by expression of KLRG1. Eur J Immunol 37(12):3445-54. [PubMed: 18034419]  [MGI Ref ID J:128529]

Brinster C; Shevach EM. 2005. Bone marrow-derived dendritic cells reverse the anergic state of CD4+CD25+ T cells without reversing their suppressive function. J Immunol 175(11):7332-40. [PubMed: 16301639]  [MGI Ref ID J:122138]

Buhlmann JE; Gonzalez M; Ginther B; Panoskaltsis-Mortari A; Blazar BR; Greiner DL; Rossini AA; Flavell R; Noelle RJ. 1999. Cutting edge: sustained expansion of CD8+ T cells requires CD154 expression by Th cells in acute graft versus host disease. J Immunol 162(8):4373-6. [PubMed: 10201970]  [MGI Ref ID J:119788]

Burchill MA; Yang J; Vogtenhuber C; Blazar BR; Farrar MA. 2007. IL-2 receptor beta-dependent STAT5 activation is required for the development of Foxp3+ regulatory T cells. J Immunol 178(1):280-90. [PubMed: 17182565]  [MGI Ref ID J:141932]

Carrier J; Medline A; Sohn KJ; Choi M; Martin R; Hwang SW; Kim YI. 2003. Effects of dietary folate on ulcerative colitis-associated colorectal carcinogenesis in the interleukin 2- and beta(2)-microglobulin-deficient mice. Cancer Epidemiol Biomarkers Prev 12(11 Pt 1):1262-7. [PubMed: 14652292]  [MGI Ref ID J:87528]

Carrier Y; Yuan J; Kuchroo VK; Weiner HL. 2007. Th3 cells in peripheral tolerance. II. TGF-beta-transgenic Th3 cells rescue IL-2-deficient mice from autoimmunity. J Immunol 178(1):172-8. [PubMed: 17182552]  [MGI Ref ID J:141942]

Chastagner P; Reddy J; Theze J. 2002. Lymphoadenopathy in IL-2-Deficient Mice: Further Characterization and Overexpression of the Antiapoptotic Molecule Cellular FLIP. J Immunol 169(7):3644-51. [PubMed: 12244156]  [MGI Ref ID J:79241]

Chen J; Astle CM; Harrison DE. 2002. Hematopoietic stem cell functional failure in interleukin-2-deficient mice. J Hematother Stem Cell Res 11(6):905-12. [PubMed: 12590705]  [MGI Ref ID J:115513]

Cho JH; Boyman O; Kim HO; Hahm B; Rubinstein MP; Ramsey C; Kim DM; Surh CD; Sprent J. 2007. An intense form of homeostatic proliferation of naive CD8+ cells driven by IL-2. J Exp Med 204(8):1787-801. [PubMed: 17664294]  [MGI Ref ID J:125917]

Contractor NV; Bassiri H; Reya T; Park AY; Baumgart DC; Wasik MA; Emerson SG; Carding SR. 1998. Lymphoid hyperplasia, autoimmunity, and compromised intestinal intraepithelial lymphocyte development in colitis-free gnotobiotic IL-2-deficient mice. J Immunol 160(1):385-94. [PubMed: 9551995]  [MGI Ref ID J:46312]

D'Cruz LM; Klein L. 2005. Development and function of agonist-induced CD25+Foxp3+ regulatory T cells in the absence of interleukin 2 signaling. Nat Immunol 6(11):1152-9. [PubMed: 16227983]  [MGI Ref ID J:112603]

D'Souza WN; Lefrancois L. 2003. IL-2 is not required for the initiation of CD8 T cell cycling but sustains expansion. J Immunol 171(11):5727-35. [PubMed: 14634080]  [MGI Ref ID J:117985]

Dai Z; Konieczny BT; Baddoura FK; Lakkis FG. 1998. Impaired alloantigen-mediated T cell apoptosis and failure to induce long-term allograft survival in IL-2-deficient mice. J Immunol 161(4):1659-63. [PubMed: 9712028]  [MGI Ref ID J:118720]

Dai Z; Konieczny BT; Lakkis FG. 2000. The dual role of IL-2 in the generation and maintenance of CD8+ memory T cells J Immunol 165(6):3031-6. [PubMed: 10975812]  [MGI Ref ID J:64553]

Demaison C; Fiette L; Blanchetiere V; Schimpl A; Theze J; Froussard P. 1998. IL-2 receptor alpha-chain expression is independently regulated in primary and secondary lymphoid organs. J Immunol 161(4):1977-82. [PubMed: 9712069]  [MGI Ref ID J:110999]

Diaz-de-Durana Y; Mantchev GT; Bram RJ; Franco A. 2006. TACI-BLyS signaling via B-cell-dendritic cell cooperation is required for naive CD8+ T-cell priming in vivo. Blood 107(2):594-601. [PubMed: 16195331]  [MGI Ref ID J:126637]

Dooms H; Kahn E; Knoechel B; Abbas AK. 2004. IL-2 induces a competitive survival advantage in T lymphocytes. J Immunol 172(10):5973-9. [PubMed: 15128779]  [MGI Ref ID J:89699]

Dooms H; Wolslegel K; Lin P; Abbas AK. 2007. Interleukin-2 enhances CD4+ T cell memory by promoting the generation of IL-7R alpha-expressing cells. J Exp Med 204(3):547-57. [PubMed: 17312008]  [MGI Ref ID J:125364]

Duffy D; Yang CP; Heath A; Garside P; Bell EB. 2006. Naive T-cell receptor transgenic T cells help memory B cells produce antibody. Immunology 119(3):376-84. [PubMed: 17067314]  [MGI Ref ID J:118532]

Ehrhardt RO; Ludviksson BR; Gray B; Neurath M; Strober W. 1997. Induction and prevention of colonic inflammation in IL-2-deficient mice. J Immunol 158(2):566-73. [PubMed: 8992969]  [MGI Ref ID J:110763]

Elias KM; Laurence A; Davidson TS; Stephens G; Kanno Y; Shevach EM; O'Shea JJ. 2008. Retinoic acid inhibits Th17 polarization and enhances FoxP3 expression through a Stat-3/Stat-5 independent signaling pathway. Blood 111(3):1013-20. [PubMed: 17951529]  [MGI Ref ID J:130685]

Enomoto T; Weghorst CM; Ward JM; Anderson LM; Perantoni AO; Rice JM. 1993. Low frequency of H-ras activation in naturally occurring hepatocellular tumors of C3H/HeNCr mice. Carcinogenesis 14(9):1939-44. [PubMed: 8403222]  [MGI Ref ID J:14839]

Feau S; Arens R; Togher S; Schoenberger SP. 2011. Autocrine IL-2 is required for secondary population expansion of CD8(+) memory T cells. Nat Immunol 12(9):908-13. [PubMed: 21804558]  [MGI Ref ID J:176468]

Fehervari Z; Sakaguchi S. 2004. Control of Foxp3+ CD25+CD4+ regulatory cell activation and function by dendritic cells. Int Immunol 16(12):1769-80. [PubMed: 15520045]  [MGI Ref ID J:94004]

Fontenot JD; Rasmussen JP; Gavin MA; Rudensky AY. 2005. A function for interleukin 2 in Foxp3-expressing regulatory T cells. Nat Immunol 6(11):1142-51. [PubMed: 16227984]  [MGI Ref ID J:112602]

French AR; Sjolin H; Kim S; Koka R; Yang L; Young DA; Cerboni C; Tomasello E; Ma A; Vivier E; Karre K; Yokoyama WM. 2006. DAP12 signaling directly augments proproliferative cytokine stimulation of NK cells during viral infections. J Immunol 177(8):4981-90. [PubMed: 17015680]  [MGI Ref ID J:139300]

Freyschmidt-Paul P; McElwee KJ; Hoffmann R; Sundberg JP; Kissling S; Hummel S; Vitacolonna M; Kopp-Schneider A; Zoller M. 2005. Reduced expression of interleukin-2 decreases the frequency of alopecia areata onset in C3H/HeJ mice. J Invest Dermatol 125(5):945-51. [PubMed: 16297194]  [MGI Ref ID J:102954]

Gaetke LM; Oz HS; de Villiers WJ; Varilek GW; Frederich RC. 2002. The leptin defense against wasting is abolished in the IL-2-deficient mouse model of inflammatory bowel disease. J Nutr 132(5):893-6. [PubMed: 11983809]  [MGI Ref ID J:76491]

Grassl G; Pummerer CL; Horak I; Neu N. 1997. Induction of autoimmune myocarditis in interleukin-2-deficient mice. Circulation 95(7):1773-6. [PubMed: 9107162]  [MGI Ref ID J:40082]

Guimond MJ; Luross JA; Wang B; Terhorst C; Danial S; Croy BA. 1997. Absence of natural killer cells during murine pregnancy is associated with reproductive compromise in TgE26 mice. Biol Reprod 56(1):169-79. [PubMed: 9002646]  [MGI Ref ID J:134589]

Guo Z; Khattar M; Schroder PM; Miyahara Y; Wang G; He X; Chen W; Stepkowski SM. 2013. A Dynamic Dual Role of IL-2 Signaling in the Two-Step Differentiation Process of Adaptive Regulatory T Cells. J Immunol 190(7):3153-62. [PubMed: 23427250]  [MGI Ref ID J:194525]

Hancock WW; Tsai TL; Madaio MP; Gasser DL. 2003. Cutting Edge: Multiple autoimmune pathways in kd/kd mice. J Immunol 171(6):2778-81. [PubMed: 12960297]  [MGI Ref ID J:85380]

Herblot S; Chastagner P; Samady L; Moreau JL; Demaison C; Froussard P; Liu X; Bonnet J; Theze J. 1999. IL-2-dependent expression of genes involved in cytoskeleton organization, oncogene regulation, and transcriptional control. J Immunol 162(6):3280-8. [PubMed: 10092780]  [MGI Ref ID J:53462]

Herold KC; Lu J; Rulifson I; Vezys V; Taub D; Grusby MJ; Bluestone JA. 1997. Regulation of C-C chemokine production by murine T cells by CD28/B7 costimulation. J Immunol 159(9):4150-3. [PubMed: 9379007]  [MGI Ref ID J:110673]

Hershko AY; Suzuki R; Charles N; Alvarez-Errico D; Sargent JL; Laurence A; Rivera J. 2011. Mast cell interleukin-2 production contributes to suppression of chronic allergic dermatitis. Immunity 35(4):562-71. [PubMed: 21982597]  [MGI Ref ID J:177651]

Hinrichs CS; Borman ZA; Cassard L; Gattinoni L; Spolski R; Yu Z; Sanchez-Perez L; Muranski P; Kern SJ; Logun C; Palmer DC; Ji Y; Reger RN; Leonard WJ; Danner RL; Rosenberg SA; Restifo NP. 2009. Adoptively transferred effector cells derived from naive rather than central memory CD8+ T cells mediate superior antitumor immunity. Proc Natl Acad Sci U S A 106(41):17469-74. [PubMed: 19805141]  [MGI Ref ID J:153682]

Hofstetter HH; Sewell DL; Liu F; Sandor M; Forsthuber T; Lehmann PV; Fabry Z. 2003. Autoreactive T cells promote post-traumatic healing in the central nervous system. J Neuroimmunol 134(1-2):25-34. [PubMed: 12507769]  [MGI Ref ID J:119263]

Horak I; Lohler J; Ma A; Smith KA. 1995. Interleukin-2 deficient mice: a new model to study autoimmunity and self-tolerance. Immunol Rev 148:35-44. [PubMed: 8825281]  [MGI Ref ID J:40087]

Hoyer KK; Kuswanto WF; Gallo E; Abbas AK. 2009. Distinct roles of helper T-cell subsets in a systemic autoimmune disease. Blood 113(2):389-95. [PubMed: 18815283]  [MGI Ref ID J:144257]

Hoyer KK; Wolslegel K; Dooms H; Abbas AK. 2007. Targeting T cell-specific costimulators and growth factors in a model of autoimmune hemolytic anemia. J Immunol 179(5):2844-50. [PubMed: 17709498]  [MGI Ref ID J:151832]

Huang H; Hao S; Li F; Ye Z; Yang J; Xiang J. 2007. CD4+ Th1 cells promote CD8+ Tc1 cell survival, memory response, tumor localization and therapy by targeted delivery of interleukin 2 via acquired pMHC I complexes. Immunology 120(2):148-59. [PubMed: 17274112]  [MGI Ref ID J:122309]

Huang Z; Meola D; Petitto JM. 2011. Loss of CNS IL-2 gene expression modifies brain T lymphocyte trafficking: Response of normal versus autoreactive Treg-deficient T cells. Neurosci Lett 499(3):213-8. [PubMed: 21669253]  [MGI Ref ID J:174310]

Hwang KW; Sweatt WB; Mashayekhi M; Palucki DA; Sattar H; Chuang E; Alegre ML. 2004. Transgenic expression of CTLA-4 controls lymphoproliferation in IL-2-deficient mice. J Immunol 173(9):5415-24. [PubMed: 15494488]  [MGI Ref ID J:93742]

Isakson SH; Katzman SD; Hoyer KK. 2012. Spontaneous autoimmunity in the absence of IL-2 is driven by uncontrolled dendritic cells. J Immunol 189(4):1585-93. [PubMed: 22778392]  [MGI Ref ID J:189759]

Khan AA; Priya S; Saha B. 2009. IL-2 regulates SEB induced toxic shock syndrome in BALB/c mice. PLoS One 4(12):e8473. [PubMed: 20041187]  [MGI Ref ID J:155944]

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Xiao S; Sung SS; Fu SM; Ju ST. 2003. Combining Fas mutation with interleukin-2 deficiency prevents Colitis and Lupus: implicating interleukin-2 for auto-reactive T cell expansion and Fas ligand for colon epithelial cell death. J Biol Chem 278(52):52730-8. [PubMed: 14525977]  [MGI Ref ID J:87085]

Xiao X; Gong W; Demirci G; Liu W; Spoerl S; Chu X; Bishop DK; Turka LA; Li XC. 2012. New insights on OX40 in the control of T cell immunity and immune tolerance in vivo. J Immunol 188(2):892-901. [PubMed: 22147766]  [MGI Ref ID J:180889]

Yamaguchi T; Kishi A; Osaki M; Morikawa H; Prieto-Martin P; Wing K; Saito T; Sakaguchi S. 2013. Construction of self-recognizing regulatory T cells from conventional T cells by controlling CTLA-4 and IL-2 expression. Proc Natl Acad Sci U S A 110(23):E2116-25. [PubMed: 23690575]  [MGI Ref ID J:197416]

Yamanouchi J; Rainbow D; Serra P; Howlett S; Hunter K; Garner VE; Gonzalez-Munoz A; Clark J; Veijola R; Cubbon R; Chen SL; Rosa R; Cumiskey AM; Serreze DV; Gregory S; Rogers J; Lyons PA; Healy B; Smink LJ; Todd JA; Peterson LB; Wicker LS; Santamaria P. 2007. Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity. Nat Genet 39(3):329-37. [PubMed: 17277778]  [MGI Ref ID J:120349]

Yamazaki S; Bonito AJ; Spisek R; Dhodapkar M; Inaba K; Steinman RM. 2007. Dendritic cells are specialized accessory cells along with TGF- for the differentiation of Foxp3+ CD4+ regulatory T cells from peripheral Foxp3 precursors. Blood 110(13):4293-302. [PubMed: 17699744]  [MGI Ref ID J:149108]

Yang F; de Villiers WJ; Lee EY; McClain CJ; Varilek GW. 1999. Increased nuclear factor-kappaB activation in colitis of interleukin-2-deficient mice. J Lab Clin Med 134(4):378-85. [PubMed: 10521084]  [MGI Ref ID J:57978]

Yang XP; Ghoreschi K; Steward-Tharp SM; Rodriguez-Canales J; Zhu J; Grainger JR; Hirahara K; Sun HW; Wei L; Vahedi G; Kanno Y; O'Shea JJ; Laurence A. 2011. Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5. Nat Immunol 12(3):247-54. [PubMed: 21278738]  [MGI Ref ID J:169304]

Zand MS; Li Y; Hancock W; Li XC; Roy-Chaudhury P; Zheng XX; Strom TB. 2000. Interleukin-2 and interferon-gamma double knockout mice reject heterotopic cardiac allografts Transplantation 70(9):1378-81. [PubMed: 11087156]  [MGI Ref ID J:65781]

Zanoni I; Spreafico R; Bodio C; Di Gioia M; Cigni C; Broggi A; Gorletta T; Caccia M; Chirico G; Sironi L; Collini M; Colombo MP; Garbi N; Granucci F. 2013. IL-15 cis presentation is required for optimal NK cell activation in lipopolysaccharide-mediated inflammatory conditions. Cell Rep 4(6):1235-49. [PubMed: 24055061]  [MGI Ref ID J:203792]

Zheng L; Sharma R; Gaskin F; Fu SM; Ju ST. 2007. A novel role of IL-2 in organ-specific autoimmune inflammation beyond regulatory T cell checkpoint: both IL-2 knockout and Fas mutation prolong lifespan of Scurfy mice but by different mechanisms. J Immunol 179(12):8035-41. [PubMed: 18056343]  [MGI Ref ID J:155041]

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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

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
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 willfulfill 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

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
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 willfulfill 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.

Control Information

  Control
   Wild-type from the colony
   000659 C3H/HeJ
 
  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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

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

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

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.


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