Overview

Also Known As: CCR7-

Homozygous mice show delayed primary B or T cell immune responses. Lymph nodes from homozygous mice are devoid of naive T cells and dendritic cells, and secondary lymph organs exhibit morphological abnormalities. These mutant mice may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs, alloimmune responses, and the development of transplant rejection.

Donating Investigator

Martin Lipp, Max-Delbrueck-Center

Genetic overview

Genetic Background	Generation
	N9+N2F2 (2019-03-18 00:00:00)

Ccr7^tm1Rfor

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Ccr7	chemokine (C-C motif) receptor 7

View Genetics

Research Applications

Immunology, Inflammation and Autoimmunity Research
Research Tools
Internal/Organ Research
Hematological Research

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Base Price

Starting at:

$231.00 Domestic price for female

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Details

Detailed Description

Homozygous mice are viable and fertile and show delayed primary B or T cell immune responses. Lymph nodes from homozygous mice are devoid of naive T cells and dendritic cells (DCs), but the T cell populations in the blood, the red pulp of the spleen, and in the bone marrow are greatly expanded. Secondary lymph organs exhibit morphological abnormalities, and adoptive transfer experiments demonstrate impaired B- and T-cell migration. In a model of acute allogeneic tumor rejection, homozygous mice fail to reject subcutaneously injected MHC class I mismatched tumor cells, and cytotoxic activity of allospecific T cells is severely compromised. These mutant mice (along with CXCR5-deficient mice - Stock No. 006659) - may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs (and their homing to T- and B-cell zones therein), alloimmune responses, and the development of transplant rejection.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

A targeting vector was designed to replace a fragment of the third exon of the targeted gene (encompassing amino acids Ser-139 to Asp-309) with a neomycin resistance gene. The construct was electroporated into 129P2/OlaHsd-derived E14K embryonic stem (ES) cells, and correctly targeted ES cells were injected into BALB/c blastocysts. Chimeric males were bred to BALB/c. Mutant mice were backcrossed to C57BL/6 mice for 8 generations prior to arrival at The Jackson Laboratory. These mice were maintained on a mixed C57BL/6J ; C57BL/6NJ congenic background. Upon arrival, sperm was cryopreserved. To establish our live colony, an aliquot of frozen sperm was used to fertilize C57BL/6J oocytes (Stock No. 000664).

In 2015, a 32 SNP (single nucleotide polymorphism) panel with markers on 14 of 19 chromosomes, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed. This revealed 3 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating.

Control Suggestions

Approximate Controls

000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Hopken UE; Droese J; Li JP; Joergensen J; Breitfeld D; Zerwes HG; Lipp M. 2004. The chemokine receptor CCR7 controls lymph node-dependent cytotoxic T cell priming in alloimmune responses. Eur J Immunol 34(2):461-70PubMed: 14768051 MGI: J:121522
Forster R; Schubel A; Breitfeld D; Kremmer E; Renner-Muller I; Wolf E; Lipp M. 1999. CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs. Cell 99(1):23-33PubMed: 10520991 MGI: J:57976

View All References

Genetics

Ccr7^tm1Rfor

Allele Symbol: Ccr7^tm1Rfor

Allele Name	targeted mutation 1, Reinhold Forster
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Ccr7^tm1Rfor; targeted mutation 1, Reinhold Forster
Gene Symbol and Name	Ccr7, chemokine (C-C motif) receptor 7
Gene Synonym(s)	CD197; BLR2; CMKBR7; Epstein-Barr virus induced gene 1 homolog; chemokine (C-C) receptor 7; EBI1; Ebi1h; CC-CKR-7; Ebi1h; CCR-7; CDw197; Cmkbr7; Cmkbr7
Strain of Origin	129P2/OlaHsd
Chromosome	11
Molecular Note	0.5 kb of exon 3 encoding serine 139 to aspartic acid 309 was disrupted by insertion of a neomycin resistance cassette via homologous recombination. Successful targeting was verified in homozygous mutant animals by Southern blot analysis and chemotaxis assays. Spleen cells from homozygous animals demonstrated lack of chemotactic response towards EBI-1 ligand chemokine (ELC), a known ligand of the targeted gene.
Mutations Made By	Martin Lipp, Max-Delbrueck-Center

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Sjogren's syndrome

Research Areas By Genotype

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

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - B cell deficiency
  - B and T cell deficiency
  - B cell defects
  - T cell deficiency
  - multiple immune defects
  - defects in humoral immune responses
- Lymphoid Tissue Defects
  - Lymphocyte Homing
  - B and T cell deficiency
- Inflammation
  - B and T cell deficiency
- CD Antigens, Antigen Receptors, and Histocompatibility Markers
  - genes regulating susceptibility to infectious disease and endotoxin
- Growth Factors/Receptors/Cytokines
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - T cell deficiency
  - genes regulating susceptibility to infectious disease and endotoxin
  - B and T cell deficiency
  - B cell deficiency
Internal/Organ Research
- Lymphoid Tissue Defects
  - B and T cell deficiency
  - T cell deficiency
Hematological Research
- Immunological Defects
  - B and T cell deficiency

Mammalian Phenotype Terms by Genotype

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

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
involves: 129P2/OlaHsd * BALB/c

cellular phenotype

abnormal leukocyte migration
- adoptive transfer experiments to wild-type recipients revealed that homozygotes display impaired migration of B cells and T cells into lymph nodes and Peyer's pathces, and of T cells into the splenic periarteriolar lymphoid sheath (PALS)
- unlike wild-type B cells, mutant B cells rapidly leave the outer PALS after being transferred into wild-type recipients

immune system phenotype

abnormal B cell activation
- at 10 weeks of age, mutant B cells isolated from blood and all secondary lymphoid organs express higher levels of MHC II molecules than wild-type B cells
- at 3 weeks of age, homozygotes harbor activated B cells (with increased expression levels of MHC II) only in peripheral lymph nodes but not in blood or spleen
- homozygotes display improper activation of B cells, as shown by an increased proportion of IgD^-IgM^low B cells in the germinal center of lymph nodes

abnormal B cell physiology
- adoptive transfer experiments revealed that mutant B cells enter the recipients'lymph nodes and Peyer's patches with a frequency of 20%-50% of that observed after transfer of wild-type cells
- unlike wild-type cells, adoptively transferred mutant B cells are not retained in the outer PALS but quickly migrate to the adjacent follicle, suggesting that temporary retention of B cells in this area and interaction with antigen-specifc T cells is perturbed
- urbed

abnormal class switch recombination
- after immunization with the T cell-dependent antigen DNP-KLH, homozygotes exhibit a significant delay in IgG isotype switching relative to similarly-treated wild-type controls

abnormal dendritic cell physiology
- following contact sensitization induced by FITC skin painting, homozygotes display impaired migration of activated skin DCs to their draining lumph nodes

abnormal humoral immune response
- following application of the T-dependent antigen DNP-KLH, homozygotes fail to produce specific antibodies of any IgG isotype within the first 10 days

abnormal leukocyte migration
- adoptive transfer experiments to wild-type recipients revealed that homozygotes display impaired migration of B cells and T cells into lymph nodes and Peyer's pathces, and of T cells into the splenic periarteriolar lymphoid sheath (PALS)
- unlike wild-type B cells, mutant B cells rapidly leave the outer PALS after being transferred into wild-type recipients

abnormal lymph node cortex morphology
- homozygotes display an abnormal distribution of B and T cells within the paracortex

abnormal lymph node germinal center morphology
- some homozygotes display prominent B cell follicles with significantly enlarged germinal centers in the paracortex

abnormal lymph node T cell domain morphology
- T cells are abnormally located toward the marginal sinus

abnormal Peyer's patch T cell area morphology
- a small rim of T cells is shown to surround the B cell follicle, not observed in wild-type mice
- mutant Peyer's patches lack T cell-rich zones

abnormal spleen marginal sinus morphology
- T cells are mislolocalized and spread throughout the marginal sinuses and the red pulp in large clusters instead of being found in the PALS

abnormal spleen periarteriolar lymphoid sheath morphology
- naive T cells reside outside the PALS in mutant mice
- unlike wild-type controls, homozygotes exhibit only very few naive CD62L⁺ T cells in the T cell zone close to the central artery; those T cells found in PALS are of the memory phenotype lacking CD62L expression

abnormal spleen red pulp morphology
- T cells are mislolocalized and spread throughout the marginal sinuses and the red pulp in large clusters instead of being found in the PALS

abnormal T cell physiology
- adoptive transfer experiments revealed that mutant T cells enter the recipients' lymph nodes and Peyer's patches with a frequency of 5% to 25% of that observed after transfer of wild-type cells
- homozygotes display impaired migration of T cells into the splenic periarteriolar lymphoid sheath (PALS)

decreased CD4-positive, alpha beta T cell number
- homozygotes show a significant reduction of CD4⁺ cell numbers in mesenteric and peripheral lymph nodes (50%-70%) and Peyer's patches (25%) relative to wild-type controls

decreased dendritic cell number
- following FITC skin painting, significantly less skin-derived DCs are found in mutant LNs relative to wild-type controls
- unlike in wild-type mice, only few, morphologically altered DCs are detected in the T cell zone of mutant lymph nodes

decreased IgG3 level

decreased susceptibility to type IV hypersensitivity reaction
- contact hypersensitivity induced by epicutaneous application of FITC in the ear lobe is completely absent, as assessed by ear swelling at 24 and 48 hrs after reexposure of sensitized homozygotes to the same antigen
- delayed type hypersensitivity induced by s.c. injection of KLH in the ear lobe is completely absent, as assessed by ear swelling at 24 and 48 hrs after reexposure of sensitized homozygotes to the same antigen

decreased T cell number
- homozygotes show a significant reduction in the percentage of CD62L⁺ naive T cells in all secondary lymphoid organs relative to wild-type controls

enlarged spleen
- mutant spleens are usually 2- to 3-fold enlarged relative to wild-type spleens

increased CD4-positive, alpha beta T cell number
- homozygotes show a 6-fold increase in CD4⁺ cell numbers in peripheral blood, spleen, and bone marrow relative to wild-type controls

increased IgE level

increased IgG1 level

increased IgG2a level

increased T cell number
- homozygotes show a significant expansion of CD62L⁺ naive T cells in blood and bone marrow relative to wild-type controls

small lymph nodes
- mutant lymph nodes are smaller than wild-type

small Peyer's patches
- mutant Peyer's patches are smaller than wild-type

hematopoietic system phenotype

abnormal B cell activation
- at 10 weeks of age, mutant B cells isolated from blood and all secondary lymphoid organs express higher levels of MHC II molecules than wild-type B cells
- at 3 weeks of age, homozygotes harbor activated B cells (with increased expression levels of MHC II) only in peripheral lymph nodes but not in blood or spleen
- homozygotes display improper activation of B cells, as shown by an increased proportion of IgD^-IgM^low B cells in the germinal center of lymph nodes

abnormal B cell physiology
- adoptive transfer experiments revealed that mutant B cells enter the recipients'lymph nodes and Peyer's patches with a frequency of 20%-50% of that observed after transfer of wild-type cells
- unlike wild-type cells, adoptively transferred mutant B cells are not retained in the outer PALS but quickly migrate to the adjacent follicle, suggesting that temporary retention of B cells in this area and interaction with antigen-specifc T cells is perturbed
- urbed

abnormal class switch recombination
- after immunization with the T cell-dependent antigen DNP-KLH, homozygotes exhibit a significant delay in IgG isotype switching relative to similarly-treated wild-type controls

abnormal leukocyte migration
- adoptive transfer experiments to wild-type recipients revealed that homozygotes display impaired migration of B cells and T cells into lymph nodes and Peyer's pathces, and of T cells into the splenic periarteriolar lymphoid sheath (PALS)
- unlike wild-type B cells, mutant B cells rapidly leave the outer PALS after being transferred into wild-type recipients

abnormal spleen marginal sinus morphology
- T cells are mislolocalized and spread throughout the marginal sinuses and the red pulp in large clusters instead of being found in the PALS

abnormal spleen periarteriolar lymphoid sheath morphology
- naive T cells reside outside the PALS in mutant mice
- unlike wild-type controls, homozygotes exhibit only very few naive CD62L⁺ T cells in the T cell zone close to the central artery; those T cells found in PALS are of the memory phenotype lacking CD62L expression

abnormal spleen red pulp morphology
- T cells are mislolocalized and spread throughout the marginal sinuses and the red pulp in large clusters instead of being found in the PALS

abnormal T cell physiology
- adoptive transfer experiments revealed that mutant T cells enter the recipients' lymph nodes and Peyer's patches with a frequency of 5% to 25% of that observed after transfer of wild-type cells
- homozygotes display impaired migration of T cells into the splenic periarteriolar lymphoid sheath (PALS)

decreased CD4-positive, alpha beta T cell number
- homozygotes show a significant reduction of CD4⁺ cell numbers in mesenteric and peripheral lymph nodes (50%-70%) and Peyer's patches (25%) relative to wild-type controls

decreased dendritic cell number
- following FITC skin painting, significantly less skin-derived DCs are found in mutant LNs relative to wild-type controls
- unlike in wild-type mice, only few, morphologically altered DCs are detected in the T cell zone of mutant lymph nodes

decreased IgG3 level

decreased T cell number
- homozygotes show a significant reduction in the percentage of CD62L⁺ naive T cells in all secondary lymphoid organs relative to wild-type controls

enlarged spleen
- mutant spleens are usually 2- to 3-fold enlarged relative to wild-type spleens

increased CD4-positive, alpha beta T cell number
- homozygotes show a 6-fold increase in CD4⁺ cell numbers in peripheral blood, spleen, and bone marrow relative to wild-type controls

increased IgE level

increased IgG1 level

increased IgG2a level

increased T cell number
- homozygotes show a significant expansion of CD62L⁺ naive T cells in blood and bone marrow relative to wild-type controls

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
involves: 129/Sv * 129P2/OlaHsd * C57BL/6

immune system phenotype

abnormal dendritic cell physiology
- dendritic cells transplanted into the footpad fail to drain into lymph nodes unlike wild-type cells

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
involves: 129P2/OlaHsd

cellular phenotype

abnormal dendritic cell chemotaxis
- very few CD103+ and CD11b^hi dendritic cells migrate to the mediastinal lymph nodes in both steady state conditions and following OVA/LPS instillation

hematopoietic system phenotype

abnormal dendritic cell chemotaxis
- very few CD103+ and CD11b^hi dendritic cells migrate to the mediastinal lymph nodes in both steady state conditions and following OVA/LPS instillation

decreased CD103-positive CD11b-low dendritic cell number
- CD103+ dendritic cells are almost absent in the mediastinal lymph nodes in both steady state conditions and following OVA/LPS instillation

decreased CD11b-high dendritic cell number
- some CD11b^hi dendritic cells are present in the mediastinal lymph nodes in both steady state conditions and following OVA/LPS inhalation, but are fewer in number than wild-type

immune system phenotype

abnormal dendritic cell chemotaxis
- very few CD103+ and CD11b^hi dendritic cells migrate to the mediastinal lymph nodes in both steady state conditions and following OVA/LPS instillation

decreased CD103-positive CD11b-low dendritic cell number
- CD103+ dendritic cells are almost absent in the mediastinal lymph nodes in both steady state conditions and following OVA/LPS instillation

decreased CD11b-high dendritic cell number
- some CD11b^hi dendritic cells are present in the mediastinal lymph nodes in both steady state conditions and following OVA/LPS inhalation, but are fewer in number than wild-type

The following phenotype relates to a compound genotype created using this strain

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
B6.129P2-Ccr7

cellular phenotype

abnormal leukocyte migration
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice
- single positive T cells are retained in the cortex of the thymus
- single positive T cells fail to localize to the medulla of the thymus in newborns

hematopoietic system phenotype

abnormal leukocyte migration
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice
- single positive T cells are retained in the cortex of the thymus
- single positive T cells fail to localize to the medulla of the thymus in newborns

abnormal thymus cortex morphology
- single positive thymocytes are retained by the cortex rather than migrating to the medulla

small thymus medulla
- medullary volume is about 50% that found in controls
- reduced in size in the adult thymus

homeostasis/metabolism phenotype

abnormal physiological response to xenobiotic
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice

immune system phenotype

abnormal dendritic cell physiology
- 18 h after stimulation by fluorescein isothiocyanate skin painting dendritic cells fail to reach the lymph nodes
- this defect can be partially overcome by use of high antigen doses

abnormal leukocyte migration
- FTY720-treated mice exhibit an accumulation of mature thymocytes in the cortex rather than medulla of the thymus as in similarly treated wild-type mice
- single positive T cells are retained in the cortex of the thymus
- single positive T cells fail to localize to the medulla of the thymus in newborns

abnormal thymus cortex morphology
- single positive thymocytes are retained by the cortex rather than migrating to the medulla

increased inflammatory response

increased susceptibility to autoimmune disorder
- mice exhibit autoimmune exocrinopathy unlike wild-type mice

lacrimal gland inflammation
- lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice
- mice exhibit dacryoadenitis unlike wild-type mice

parotid gland inflammation
- parotid glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

salivary gland inflammation
- mice exhibit sialadenitis unlike wild-type mice

small thymus medulla
- medullary volume is about 50% that found in controls
- reduced in size in the adult thymus

submandibular gland inflammation
- submandicular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

digestive/alimentary phenotype

abnormal parotid gland morphology
- mice exhibit parotid gland tissue damage associated with inflammation unlike wild-type mice

abnormal submandibular gland morphology
- mice exhibit submandibular gland tissue damage associated with inflammation unlike wild-type mice

parotid gland inflammation
- parotid glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

salivary gland inflammation
- mice exhibit sialadenitis unlike wild-type mice

submandibular gland inflammation
- submandicular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

mammalian phenotype

immune system phenotype
- Normal - no single positive T cell abnormalities other than the migration defect from cortex to medulla of the thymus

vision/eye phenotype

abnormal lacrimal gland morphology
- lacrimal glands exhibit periductal lymphocyte infiltration causing destruction of acinar cells unlike in wild-type mice

lacrimal gland inflammation
- lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice
- mice exhibit dacryoadenitis unlike wild-type mice

endocrine/exocrine gland phenotype

abnormal exocrine gland morphology
- as early as 5 weeks of age, mice exhibit lesions in exocrine glands unlike wild-type mice

abnormal lacrimal gland morphology
- lacrimal glands exhibit periductal lymphocyte infiltration causing destruction of acinar cells unlike in wild-type mice

abnormal parotid gland morphology
- mice exhibit parotid gland tissue damage associated with inflammation unlike wild-type mice

abnormal submandibular gland morphology
- mice exhibit submandibular gland tissue damage associated with inflammation unlike wild-type mice

abnormal thymus cortex morphology
- single positive thymocytes are retained by the cortex rather than migrating to the medulla

lacrimal gland inflammation
- lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice
- mice exhibit dacryoadenitis unlike wild-type mice

parotid gland inflammation
- parotid glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

salivary gland inflammation
- mice exhibit sialadenitis unlike wild-type mice

small thymus medulla
- medullary volume is about 50% that found in controls
- reduced in size in the adult thymus

submandibular gland inflammation
- submandicular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
B6.129P2(C)-Ccr7/J

immune system phenotype

decreased susceptibility to bacterial infection
- mice treated with antibiotic to remove commensal bacteria and infected with non-invasive Salmonella exhibit decreased bacterial titers in the mesenteric lymph nodes as compared to wild type controls

References

Hopken UE; Droese J; Li JP; Joergensen J; Breitfeld D; Zerwes HG; Lipp M. 2004. The chemokine receptor CCR7 controls lymph node-dependent cytotoxic T cell priming in alloimmune responses. Eur J Immunol 34(2):461-70PubMed: 14768051 MGI: J:121522
Forster R; Schubel A; Breitfeld D; Kremmer E; Renner-Muller I; Wolf E; Lipp M. 1999. CCR7 coordinates the primary immune response by establishing functional microenvironments in secondary lymphoid organs. Cell 99(1):23-33PubMed: 10520991 MGI: J:57976

Additional - Ccr7^tm1Rfor related

Technical Support

Contact Technical Support

Genotyping Protocols
- MELT: Ccr7^tm1Rfor Alt1
- Genotyping resources and troubleshooting
Dietary Information
- New Diet as of March 2015: Lab Diet® 5K0Q (6% fat)
Breeding Considerations

When maintaining a live colony, homozygous mice are bred.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the CCR7- mouse strain in a publication, please cite the originating article(s) and include JAX stock #006621 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

Available

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Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	Heterozygous for Ccr7<tm1Rfor>

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We 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.

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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Also Known As: CCR7-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Ccr7tm1Rfor

Allele Symbol: Ccr7tm1Rfor

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Genotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Ccr7tm1Rfor/Ccr7tm1Rforinvolves: 129P2/OlaHsd * BALB/c

cellular phenotype

immune system phenotype

hematopoietic system phenotype

Genotype: Ccr7tm1Rfor/Ccr7tm1Rforinvolves: 129/Sv * 129P2/OlaHsd * C57BL/6

immune system phenotype

Genotype: Ccr7tm1Rfor/Ccr7tm1Rforinvolves: 129P2/OlaHsd

cellular phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Ccr7tm1Rfor/Ccr7tm1RforB6.129P2-Ccr7

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

digestive/alimentary phenotype

mammalian phenotype

vision/eye phenotype

endocrine/exocrine gland phenotype

Genotype: Ccr7tm1Rfor/Ccr7tm1RforB6.129P2(C)-Ccr7/J

immune system phenotype

References

Additional - Ccr7tm1Rfor related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

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Ccr7^tm1Rfor

Allele Symbol: Ccr7^tm1Rfor

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
involves: 129P2/OlaHsd * BALB/c

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
involves: 129/Sv * 129P2/OlaHsd * C57BL/6

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
involves: 129P2/OlaHsd

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
B6.129P2-Ccr7

Genotype: Ccr7^tm1Rfor/Ccr7^tm1Rfor
B6.129P2(C)-Ccr7/J

Additional - Ccr7^tm1Rfor related