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Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Background Strain C3H/HeJ Donor Strain B6;129P-Il2tm1Hor (129P2 derived E14TG2a ES cell line) Generation N10F16N1 Donating Investigator Ivan Horak, Forschungs institut fur Molekulare Appearance
agouti
Related Genotype: A/ADescription
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 | ||
|---|---|---|
| Wild-type from the colony | ||
| 000659 C3H/HeJ | ||
| Considerations for Choosing Controls | ||
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 View Strains carrying other alleles of Il2 (2 strains)
Congenic Nomenclature
JAX® NOTES, Fall 1996; 467. Il2tm1Hor, an Interleukin-2 Gene Targeted Mutation.
View Related Disease (OMIM) Terms
Related Disease (OMIM) Terms
Inflammatory Bowel Disease 1; IBD1 - Models with phenotypic similarity to human disease where etiologies are distinct.2
2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
Il2tm1Hor/Il2tm1Hor
C3.129P2-Il2tm1Hor
- hematopoietic system phenotype
- increased CD4-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion
- increased CD8-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin
- immune system phenotype
- increased CD4-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion
- increased CD8-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Il2tm1Hor/Il2tm1Hor
involves: 129P2/OlaHsd * C57BL/6
- life span-post-weaning/aging
- premature death (MGI Ref ID J:15223)
- about of 50% of mice die within the first 9 weeks of age with enlarged lymphoid organs and severe anemia
- the remaining mice die by 25 weeks of age from inflammatory bowel disease
- digestive/alimentary phenotype
- abnormal intestinal epithelium morphology (MGI Ref ID J:15223)
- prominent epithelial regeneration with crypt branching and dysplasia near areas of inflammation
- crypt hyperplasia and unusual branching is observed
- abnormal intestinal goblet cells (MGI Ref ID J:15223)
- colon epithelium shows loss of goblet cells
- loss of mucin is observed in goblet cells
- crypts of Lieberkuhn abscesses (MGI Ref ID J:15223)
- frequently occurres in the large intestine
- intestinal ulcer (MGI Ref ID J:15223)
- ulcers occur in the large intestine, with pronounced thickening of the bowel wall
- colitis (MGI Ref ID J:15223)
- 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
- infiltrating lymphocytes sometimes form nodules
- mice bred in a germ-free facility do not display any histopathological signs of colitis
- 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
- occurs in all mice that survive past 9 weeks of age, with thickening of large intestinal wall
- mice kept under a specific pathogen free environment develop colitis when immunized with an antigen that activates CD4 T cells
- diarrhea (MGI Ref ID J:29999)
- occurs in mice 24 weeks of age
- chronic diarrhea (MGI Ref ID J:15223)
- all mice that do not die within the first 9 weeks after birth exhibit diarrhea
- rectal hemorrhage (MGI Ref ID J:29999)
- rarely observed
- rectal prolapse (MGI Ref ID J:29999)
- occasional occurrence among mice whom live past 9 weeks of age
- frequent occurrence among mice whom live past 9 weeks of age
- immune system phenotype
- abnormal immune system organ morphology (MGI Ref ID J:79241)
- proliferative response of splenocytes to anti-CD3 antibody is only 16% of wt controls
- poor proliferative response to anti-CD3 antibody is partially rescued by addition of cytokines including IL-2, IL-4, IL-7
- there is reduced proliferation to allogenic leukocytes
- enlarged lymph nodes (MGI Ref ID J:15223)
- lymph node hyperplasia (MGI Ref ID J:16662)
- enlarged mesenteric lymph nodes (MGI Ref ID J:29999)
- increased 3-10 fold in size as compared to control littermates
- enlarged spleen (MGI Ref ID J:15223)
- occurs in the 50% of mice that die prematurely
- abnormal lymphocyte morphology (MGI Ref ID J:37220)
- decreased apoptosis in thymus upon injection with anti-CD3 antibody
- abnormal CD8 positive, alpha-beta intraepithelial T cell morphology (MGI Ref ID J:15223)
- increased number (5-100 fold) are found in diseased colon
- T cells expressing the CD8 alpha-beta heterodimer predominate over CD8 alpha-alpha T cells
- abnormal T-helper 1 cell differentiation (MGI Ref ID J:37220)
- 10 fold greater amounts of IFN gamma were made by thymocytes from immunized mutant mice as measured by an in vitro assay
- low levels of the Th2 cytokine IL-4 were made compared to the large level made by wt thymocytes
- however, treatment with an IL-12 neutralizing antibody normalized Th1cytokine levels
- abnormal class switch recombination (MGI Ref ID J:15573)
- there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus
- abnormal gamma-delta intraepithelial T cell morphology (MGI Ref ID J:15223)
- decreased percentage of these cells are found in the colon epithelium
- abnormal lymphocyte cell number (MGI Ref ID J:15223)
- decreased double-negative T cell number (MGI Ref ID J:15223)
- there is a drastic reduction in the colon
- decreased double-positive T cell number (MGI Ref ID J:37220)
- 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
- increased double-negative T cell number (MGI Ref ID J:37220)
- 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
- increased pre-B cell number (MGI Ref ID J:16662)
- of cells in the bone marrow
- increased single-positive T cell number (MGI Ref ID J:37220)
- 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
- however, treatment with an IL-12 neutralizing antibody normalized SP cell numbers
- abnormal thymocyte activation (MGI Ref ID J:37220)
- increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1
- however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes
- in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody
- decreased T cell proliferation (MGI Ref ID J:26198)
- increased B cell proliferation (MGI Ref ID J:16662)
- B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate
- increased T cell proliferation (MGI Ref ID J:15223)
- the proliferation of T cells in the colon is twice that of wild-type controls
- 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate
- increased pro-B cell number (MGI Ref ID J:16662)
- of cells in the bone marrow
- abnormal lymphocyte physiology (MGI Ref ID J:15223)
- abnormal CD4-positive T cell physiology (MGI Ref ID J:15573)
- there is an impaired ability to induce Ig class switching in B cells after infection with vesicular stomatitis virus
- increased cytotoxic effectiveness of CD4 T cells isolated from the colon
- unable to induce IgM secretion from activated B cells in an in vitro assay
- however, IgM levels are in vivo are normal
- abnormal class switch recombination (MGI Ref ID J:15573)
- there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus
- abnormal cytotoxic T cell physiology (MGI Ref ID J:39981)
- enhanced target cell killing by intraepithelial lymphocytes T cells (IEL) and lamina propia lymphocytes of the large intestine
- enhanced target cell killing by intraepithelial lymphocytes T cells (IEL) of the small intestine
- defective cytotoxic T cell cytolysis (MGI Ref ID J:15573)
- there is a three fold reduction of target cell killing by primary T cells in a chromium release assay
- no target cell killing by previously stimulated T cells in a chromium release assay
- there is reduced killing of allogeneic tumor cells in an in vitro assay
- footpad swelling is reduced 6-10 days after infection with lymphocytic choriomeningitis virus
- abnormal level of surface class II molecules (MGI Ref ID J:15223)
- expression occurs in high number of colon epithelial cells
- abnormal thymocyte activation (MGI Ref ID J:37220)
- increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1
- however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes
- in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody
- decreased T cell proliferation (MGI Ref ID J:26198)
- impaired NK cell cytolysis (MGI Ref ID J:15573)
- 3 to 9 fold reduction in killing of NK susceptible target cells as measured by chromium release assay
- increased B cell proliferation (MGI Ref ID J:16662)
- B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate
- increased IgA level (MGI Ref ID J:15223)
- drastic elevation in secretion by B cells found in the colon
- increased IgE level (MGI Ref ID J:16662)
- levels are 10 fold higher than those observed in wild-type mice
- increased IgG1 level (MGI Ref ID J:15223)
- drastic elevation in secretion of IgG1 by B cells found in the colon
- levels of IgG1 are increased 100 fold
- levels of IgG1 are drastically increased to levels above 2700 ug/ml
- increased IgG2a level (MGI Ref ID J:16662)
- levels of IgG2a are also elevated
- increased IgG2b level (MGI Ref ID J:16662)
- levels of IgG2b are also elevated
- increased T cell proliferation (MGI Ref ID J:15223)
- the proliferation of T cells in the colon is twice that of wild-type controls
- 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate
- colitis (MGI Ref ID J:15223)
- 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
- infiltrating lymphocytes sometimes form nodules
- mice bred in a germ-free facility do not display any histopathological signs of colitis
- 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
- occurs in all mice that survive past 9 weeks of age, with thickening of large intestinal wall
- mice kept under a specific pathogen free environment develop colitis when immunized with an antigen that activates CD4 T cells
- increased length of allograft survival (MGI Ref ID J:26198)
- graft rejection of allogeneic pancreatic islet cells is delayed by 11 days compared to controls
- increased susceptibility to viral infection (MGI Ref ID J:26861)
- despite reduced cytotoxic T cell activity, mice still clear lymphocytic choriomeningitis virus within nine days of infection
- other phenotype
- amyloidosis (MGI Ref ID J:15223)
- predominately in liver, spleen, and kidneys
- growth/size phenotype
- cachexia (MGI Ref ID J:29999)
- weight loss resulting from intestinal inflammation is observed by 24 weeks
- hematopoietic system phenotype
- abnormal lymphocyte morphology (MGI Ref ID J:37220)
- decreased apoptosis in thymus upon injection with anti-CD3 antibody
- abnormal CD8 positive, alpha-beta intraepithelial T cell morphology (MGI Ref ID J:15223)
- increased number (5-100 fold) are found in diseased colon
- T cells expressing the CD8 alpha-beta heterodimer predominate over CD8 alpha-alpha T cells
- abnormal T-helper 1 cell differentiation (MGI Ref ID J:37220)
- 10 fold greater amounts of IFN gamma were made by thymocytes from immunized mutant mice as measured by an in vitro assay
- low levels of the Th2 cytokine IL-4 were made compared to the large level made by wt thymocytes
- however, treatment with an IL-12 neutralizing antibody normalized Th1cytokine levels
- abnormal class switch recombination (MGI Ref ID J:15573)
- there is delayed class switching from IgM to IgG after infection with vesicular stomatitis virus
- abnormal gamma-delta intraepithelial T cell morphology (MGI Ref ID J:15223)
- decreased percentage of these cells are found in the colon epithelium
- abnormal lymphocyte cell number (MGI Ref ID J:15223)
- decreased double-negative T cell number (MGI Ref ID J:15223)
- there is a drastic reduction in the colon
- decreased double-positive T cell number (MGI Ref ID J:37220)
- 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
- increased double-negative T cell number (MGI Ref ID J:37220)
- 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
- increased pre-B cell number (MGI Ref ID J:16662)
- of cells in the bone marrow
- increased single-positive T cell number (MGI Ref ID J:37220)
- 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
- however, treatment with an IL-12 neutralizing antibody normalized SP cell numbers
- abnormal thymocyte activation (MGI Ref ID J:37220)
- increased activation of thymocytes 7 days after immunization with a CD4 T cell activating antigen, as measured by expression of CD69 and Icam1
- however, treatment with an IL-12 neutralizing antibody normalized the percentage of activated thymocytes
- in vitro proliferation is reduced in presence of concanavalin A or anti-CD3 antibody
- decreased T cell proliferation (MGI Ref ID J:26198)
- increased B cell proliferation (MGI Ref ID J:16662)
- B cells from lymph nodes have a larger size and incorporate more BrdU, indicating a faster proliferation rate
- increased T cell proliferation (MGI Ref ID J:15223)
- the proliferation of T cells in the colon is twice that of wild-type controls
- 2-10 fold higher using in vivo incorporation of BrdU, which indicates a faster proliferation rate
- increased pro-B cell number (MGI Ref ID J:16662)
- of cells in the bone marrow
- anemia (MGI Ref ID J:15223)
- severe anemia is found in 50% of mice that die prematurely
- occurs in mice 24 weeks of age
- enlarged spleen (MGI Ref ID J:15223)
- occurs in the 50% of mice that die prematurely
- endocrine/exocrine gland phenotype
- crypts of Lieberkuhn abscesses (MGI Ref ID J:15223)
- frequently occurres in the large intestine
- behavior/neurological phenotype
- hunched posture (MGI Ref ID J:29999)
- occurs in mice 24 weeks of age
- cardiovascular system phenotype
- rectal hemorrhage (MGI Ref ID J:29999)
- rarely observed
Il2tm1Hor/Il2tm1Hor
C.129P2-Il2tm1Hor
- life span-post-weaning/aging
- premature death (MGI Ref ID J:29799)
- 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
- immune system phenotype
- abnormal lymphocyte morphology (MGI Ref ID J:29799)
- increased B cell proliferation (MGI Ref ID J:29799)
- faster proliferation as measured by BrdU incorporation
- increased T cell proliferation (MGI Ref ID J:29799)
- by 10 days of age, T cells in lymph nodes express high levels of activation markers and are proliferating at an increased rate
- CD4 T cells are activated prior to CD8 T cells (10 days vs. 15 days of age)
- increased germinal center B cell number (MGI Ref ID J:29799)
- increased plasma cell number (MGI Ref ID J:29799)
- seen in the spleen by 15 days of age
- abnormal regulatory T cell physiology (MGI Ref ID J:112603)
- there is a rapid loss of adoptively transferred regulatory T cells
- abnormal spleen morphology (MGI Ref ID J:29799)
- increased spleen red pulp amount (MGI Ref ID J:29799)
- spleen hyperplasia (MGI Ref ID J:29799)
- 15 day old mice exhibit hyperplasia of the white pulp
- enlarged lymph nodes (MGI Ref ID J:29799)
- increased IgG level (MGI Ref ID J:29799)
- increased level of IgG secreting B cells from spleen and lymph nodes
- increased inflammatory response (MGI Ref ID J:29799)
- heart inflammation (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
- liver inflammation (MGI Ref ID J:29799)
- lung inflammation (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
- pancreas inflammation (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
- vasculitis (MGI Ref ID J:29799)
- moderate to severe inflammation noted in the major thoracic blood vessels upon necropsy
- increased susceptibility to autoimmune hemolytic anemia (MGI Ref ID J:29799)
- 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
- hematopoietic system phenotype
- abnormal bone marrow cell number (MGI Ref ID J:29799)
- invasion of T cells occur, with a concurrent drop in B cells and other nucleated cells
- abnormal lymphocyte morphology (MGI Ref ID J:29799)
- increased B cell proliferation (MGI Ref ID J:29799)
- faster proliferation as measured by BrdU incorporation
- increased T cell proliferation (MGI Ref ID J:29799)
- by 10 days of age, T cells in lymph nodes express high levels of activation markers and are proliferating at an increased rate
- CD4 T cells are activated prior to CD8 T cells (10 days vs. 15 days of age)
- increased germinal center B cell number (MGI Ref ID J:29799)
- increased plasma cell number (MGI Ref ID J:29799)
- seen in the spleen by 15 days of age
- abnormal reticulocyte morphology (MGI Ref ID J:29799)
- marked reduction concurrent with T cell invasion of marrow
- abnormal spleen morphology (MGI Ref ID J:29799)
- increased spleen red pulp amount (MGI Ref ID J:29799)
- spleen hyperplasia (MGI Ref ID J:29799)
- 15 day old mice exhibit hyperplasia of the white pulp
- decreased hematocrit (MGI Ref ID J:29799)
- increased mean corpuscular hemoglobin (MGI Ref ID J:29799)
- about twice normal levels, this indicates a hyperchromic anemia
- increased susceptibility to autoimmune hemolytic anemia (MGI Ref ID J:29799)
- 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
- 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 (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
- vasculitis (MGI Ref ID J:29799)
- moderate to severe inflammation noted in the major thoracic blood vessels upon necropsy
- digestive/alimentary phenotype
- pancreas inflammation (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
- endocrine/exocrine gland phenotype
- pancreas inflammation (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
- liver/biliary system phenotype
- liver inflammation (MGI Ref ID J:29799)
- respiratory system phenotype
- lung inflammation (MGI Ref ID J:29799)
- moderate to severe inflammation noted upon necropsy
Il2tm1Hor/Il2tm1Hor
B6.129P2-Il2tm1Hor
- immune system phenotype
- *normal* immune system phenotype (MGI Ref ID J:125748)
- 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
- increased T cell number (MGI Ref ID J:125748)
- increased CD4-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion
- increased CD8-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin
- increased activated T cell number (MGI Ref ID J:28924)
- higher numbers due to less sensitivity to Fas-mediated cell death (apoptosis)
- increased T cell proliferation (MGI Ref ID J:28924)
- T cells continue to respond to antigen instead of going into anergy during secondary stimulation with antigens
- hematopoietic system phenotype
- increased T cell number (MGI Ref ID J:125748)
- increased CD4-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers fail to decrease to normal levels after immunization with staphylococcal enterotoxin, indicating a problem with peripheral deletion
- increased CD8-positive T cell number (MGI Ref ID J:28924)
- activated T cell numbers decrease with slower kinetics than wild-type mice after after immunization with staphylococcal enterotoxin
- increased activated T cell number (MGI Ref ID J:28924)
- higher numbers due to less sensitivity to Fas-mediated cell death (apoptosis)
- increased T cell proliferation (MGI Ref ID J:28924)
- T cells continue to respond to antigen instead of going into anergy during secondary stimulation with antigens
Il2tm1Hor/Il2tm1Hor
B6.129P2-Il2tm1Hor/J
- immune system phenotype
- abnormal response to transplant (MGI Ref ID J:113547)
- wild-type regulatory T cells fail to engraft when adoptively transferred into these mice
- decreased regulatory T cell number (MGI Ref ID J:113547)
- there is a 2 to 5 fold reduction in the percentage of CD25-postive CD4 T cells in both the thymus and lymph nodes
- enlarged lymph nodes (MGI Ref ID J:113547)
- increased cellularity of lymph nodes compared to wild-type mice, but lower than what is observed in Il2rbtm1Mak mice
- increased susceptibility to autoimmune disorder (MGI Ref ID J:113547)
- generalized symptoms of autoimmunity noted at 4 weeks of age
- transfer of wild-type regulatory T cells did not prevent autoimmune disorder
- hematopoietic system phenotype
- decreased regulatory T cell number (MGI Ref ID J:113547)
- there is a 2 to 5 fold reduction in the percentage of CD25-postive CD4 T cells in both the thymus and lymph nodes
Il2tm1Hor/Il2tm1Hor
involves: 129P2/OlaHsd
- reproductive system phenotype
- *normal* reproductive system phenotype (MGI Ref ID J:134589)
- 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
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Il2tm1Hor relatedImmunology and Inflammation Research
Inflammation (Inflammatory bowel disease)
Cancer Research
Growth Factors/Receptors/Cytokines
Hematological Research
Anemia, Iron Deficiency and Transport Defects (hemolytic)
Immunological Defects
Immunology and Inflammation Research
Autoimmunity (hemolytic anemia)
Growth Factors/Receptors/Cytokines
| Allele Symbol | Il2tm1Hor | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Ivan Horak | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | IL-2 KO; IL-2-; IL-2null; Il2-; | ||
| Mutation Made By | Ivan Horak, Forschungs institut fur Molekulare | ||
| Strain of Origin | 129P2/OlaHsd | ||
| ES Cell Line Name | E14 | ||
| ES Cell Line Strain | 129P2/OlaHsd | ||
| Gene Symbol and Name | Il2, interleukin 2 | ||
| Chromosome | 3 | ||
| Gene Common Name(s) | IL-2; Il-2; TCGF; lymphokine; | ||
| 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 Protocols
Il2tm1Hor, STD PCR, vers. 1
Helpful Links
Optimizing PCR Protocols
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]
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 relatedAlmeida 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]
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Colony Maintenance
Diet Information LabDiet® 5K52/5K67
| Pricing for USA, Canada and Mexico shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 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.
| Pricing for International shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 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 for further information. |
|---|---|
| Supply Notes |
|
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 000659 C3H/HeJ | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Purchasing Information
JAX® Mice Orders
Surgical Services
Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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