Strain Name:

B6.129P2(C)-Ccr7tm1Rfor/J

Stock Number:

006621

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Availability:

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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.

Description

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.
Mating SystemHomozygote x Homozygote         (Female x Male)   15-DEC-07
Specieslaboratory mouse
GenerationN9+N1F2 (10-DEC-13)
Generation Definitions
 
Donating Investigator Martin Lipp,   Max-Delbrueck-Center

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 are maintained on a mixed C57BL/6J ; C57BL/6NJ congenic background.

Control Information

  Control
   000664 C57BL/6J (approximate)
   005304 C57BL/6NJ (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Ccr7
005794   B6.129P2-Ccr7tm1Dgen/J
View Strains carrying other alleles of Ccr7     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.
Sjogren Syndrome
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ccr7tm1Rfor/Ccr7tm1Rfor

        B6.129P2-Ccr7tm1Rfor
  • immune system phenotype
  • *normal* immune system phenotype
    • no single positive T cell abnormalities other than the migration defect from cortex to medulla of the thymus   (MGI Ref ID J:93960)
    • abnormal dendritic cell physiology
      • 18 h after stimulation by fluorescein isothiocyanate skin painting dendritic cells fail to reach the lymph nodes   (MGI Ref ID J:183989)
      • this defect can be partially overcome by use of high antigen doses   (MGI Ref ID J:183989)
    • abnormal leukocyte migration
      • single positive T cells fail to localize to the medulla of the thymus in newborns   (MGI Ref ID J:93960)
      • single positive T cells are retained in the cortex of the thymus   (MGI Ref ID J:93960)
      • 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   (MGI Ref ID J:110910)
    • abnormal thymus cortex morphology
      • single positive thymocytes are retained by the cortex rather than migrating to the medulla   (MGI Ref ID J:93960)
    • abnormal thymus medulla morphology
      • reduced in size in the adult thymus   (MGI Ref ID J:93960)
      • medullary volume is about 50% that found in controls   (MGI Ref ID J:93960)
    • increased inflammatory response
      • mice exhibit periductal lymphocyte infiltration in the lacrimal, parotid, and submandibular glands unlike wild-type mice   (MGI Ref ID J:110910)
      • lacrimal gland inflammation
        • lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice   (MGI Ref ID J:110910)
        • mice exhibit dacryoadenitis unlike wild-type mice   (MGI Ref ID J:110910)
      • salivary gland inflammation
        • parotid and submandicular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice   (MGI Ref ID J:110910)
        • mice exhibit sialadenitis unlike wild-type mice   (MGI Ref ID J:110910)
    • increased susceptibility to autoimmune disorder
      • mice exhibit autoimmune exocrinopathy unlike wild-type mice   (MGI Ref ID J:110910)
  • endocrine/exocrine gland phenotype
  • abnormal gland morphology
    • as early as 5 weeks of age, mice exhibit lesions in exocrine glands unlike wild-type mice   (MGI Ref ID J:110910)
    • abnormal lacrimal gland morphology
      • lacrimal glands exhibit periductal lymphocyte infiltration causing destruction of acinar cells unlike in wild-type mice   (MGI Ref ID J:110910)
    • abnormal parotid gland morphology
      • mice exhibit parotid gland tissue damage associated with inflammation unlike wild-type mice   (MGI Ref ID J:110910)
    • abnormal submandibular gland morphology
      • mice exhibit submandibular gland tissue damage associated with inflammation unlike wild-type mice   (MGI Ref ID J:110910)
    • abnormal thymus cortex morphology
      • single positive thymocytes are retained by the cortex rather than migrating to the medulla   (MGI Ref ID J:93960)
    • abnormal thymus medulla morphology
      • reduced in size in the adult thymus   (MGI Ref ID J:93960)
      • medullary volume is about 50% that found in controls   (MGI Ref ID J:93960)
  • lacrimal gland inflammation
    • lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice   (MGI Ref ID J:110910)
    • mice exhibit dacryoadenitis unlike wild-type mice   (MGI Ref ID J:110910)
  • salivary gland inflammation
    • parotid and submandicular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice   (MGI Ref ID J:110910)
    • mice exhibit sialadenitis unlike wild-type mice   (MGI Ref ID J:110910)
  • digestive/alimentary phenotype
  • abnormal parotid gland morphology
    • mice exhibit parotid gland tissue damage associated with inflammation unlike wild-type mice   (MGI Ref ID J:110910)
  • abnormal submandibular gland morphology
    • mice exhibit submandibular gland tissue damage associated with inflammation unlike wild-type mice   (MGI Ref ID J:110910)
  • salivary gland inflammation
    • parotid and submandicular glands exhibit periductal lymphocyte infiltration unlike in wild-type mice   (MGI Ref ID J:110910)
    • mice exhibit sialadenitis unlike wild-type mice   (MGI Ref ID J:110910)
  • hematopoietic system phenotype
  • abnormal leukocyte migration
    • single positive T cells fail to localize to the medulla of the thymus in newborns   (MGI Ref ID J:93960)
    • single positive T cells are retained in the cortex of the thymus   (MGI Ref ID J:93960)
    • 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   (MGI Ref ID J:110910)
  • abnormal thymus cortex morphology
    • single positive thymocytes are retained by the cortex rather than migrating to the medulla   (MGI Ref ID J:93960)
  • abnormal thymus medulla morphology
    • reduced in size in the adult thymus   (MGI Ref ID J:93960)
    • medullary volume is about 50% that found in controls   (MGI Ref ID J:93960)
  • 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   (MGI Ref ID J:110910)
  • vision/eye phenotype
  • abnormal lacrimal gland morphology
    • lacrimal glands exhibit periductal lymphocyte infiltration causing destruction of acinar cells unlike in wild-type mice   (MGI Ref ID J:110910)
  • lacrimal gland inflammation
    • lacrimal glands exhibit periductal lymphocyte infiltration unlike in wild-type mice   (MGI Ref ID J:110910)
    • mice exhibit dacryoadenitis unlike wild-type mice   (MGI Ref ID J:110910)
  • cellular phenotype
  • abnormal leukocyte migration
    • single positive T cells fail to localize to the medulla of the thymus in newborns   (MGI Ref ID J:93960)
    • single positive T cells are retained in the cortex of the thymus   (MGI Ref ID J:93960)
    • 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   (MGI Ref ID J:110910)

Ccr7tm1Rfor/Ccr7tm1Rfor

        B6.129P2(C)-Ccr7tm1Rfor/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   (MGI Ref ID J:210086)

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

Ccr7tm1Rfor/Ccr7tm1Rfor

        involves: 129P2/OlaHsd * BALB/c
  • immune system phenotype
  • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
    • abnormal B cell activation
      • homozygotes display improper activation of B cells, as shown by an increased proportion of IgD-IgMlow B cells in the germinal center of lymph nodes   (MGI Ref ID J:57976)
      • 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   (MGI Ref ID J:57976)
      • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
    • decreased IgG3 level   (MGI Ref ID J:57976)
    • increased IgE level   (MGI Ref ID J:57976)
    • increased IgG1 level   (MGI Ref ID J:57976)
    • increased IgG2a level   (MGI Ref ID J:57976)
  • abnormal Peyer's patch T cell area morphology
    • mutant Peyer's patches lack T cell-rich zones   (MGI Ref ID J:57976)
    • a small rim of T cells is shown to surround the B cell follicle, not observed in wild-type mice   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
    • homozygotes display impaired migration of T cells into the splenic periarteriolar lymphoid sheath (PALS)   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
    • decreased IgG3 level   (MGI Ref ID J:57976)
    • increased IgE level   (MGI Ref ID J:57976)
    • increased IgG1 level   (MGI Ref ID J:57976)
    • increased IgG2a level   (MGI Ref ID J:57976)
  • 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)   (MGI Ref ID J:57976)
    • unlike wild-type B cells, mutant B cells rapidly leave the outer PALS after being transferred into wild-type recipients   (MGI Ref ID J:57976)
  • abnormal lymph node cortex morphology
    • homozygotes display an abnormal distribution of B and T cells within the paracortex   (MGI Ref ID J:57976)
    • abnormal lymph node T cell domain morphology
      • T cells are abnormally located toward the marginal sinus   (MGI Ref ID J:57976)
    • abnormal lymph node germinal center morphology
      • some homozygotes display prominent B cell follicles with significantly enlarged germinal centers in the paracortex   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
  • abnormal spleen periarteriolar lymphoid sheath morphology
    • 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   (MGI Ref ID J:57976)
    • naive T cells reside outside the PALS in mutant mice   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
  • decreased dendritic cell number
    • unlike in wild-type mice, only few, morphologically altered DCs are detected in the T cell zone of mutant lymph nodes   (MGI Ref ID J:57976)
    • following FITC skin painting, significantly less skin-derived DCs are found in mutant LNs relative to wild-type controls   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
  • enlarged spleen
    • mutant spleens are usually 2- to 3-fold enlarged relative to wild-type spleens   (MGI Ref ID J:57976)
  • increased T cell number
    • homozygotes show a significant expansion of CD62L+ naive T cells in blood and bone marrow relative to wild-type controls   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
  • small Peyer's patches
    • mutant Peyer's patches are smaller than wild-type   (MGI Ref ID J:57976)
  • small lymph nodes
    • mutant lymph nodes are smaller than wild-type   (MGI Ref ID J:57976)
  • hematopoietic system phenotype
  • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
    • abnormal B cell activation
      • homozygotes display improper activation of B cells, as shown by an increased proportion of IgD-IgMlow B cells in the germinal center of lymph nodes   (MGI Ref ID J:57976)
      • 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   (MGI Ref ID J:57976)
      • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
    • decreased IgG3 level   (MGI Ref ID J:57976)
    • increased IgE level   (MGI Ref ID J:57976)
    • increased IgG1 level   (MGI Ref ID J:57976)
    • increased IgG2a level   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
    • homozygotes display impaired migration of T cells into the splenic periarteriolar lymphoid sheath (PALS)   (MGI Ref ID J:57976)
  • 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)   (MGI Ref ID J:57976)
    • unlike wild-type B cells, mutant B cells rapidly leave the outer PALS after being transferred into wild-type recipients   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
  • abnormal spleen periarteriolar lymphoid sheath morphology
    • 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   (MGI Ref ID J:57976)
    • naive T cells reside outside the PALS in mutant mice   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
  • 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   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
  • decreased dendritic cell number
    • unlike in wild-type mice, only few, morphologically altered DCs are detected in the T cell zone of mutant lymph nodes   (MGI Ref ID J:57976)
    • following FITC skin painting, significantly less skin-derived DCs are found in mutant LNs relative to wild-type controls   (MGI Ref ID J:57976)
  • enlarged spleen
    • mutant spleens are usually 2- to 3-fold enlarged relative to wild-type spleens   (MGI Ref ID J:57976)
  • increased T cell number
    • homozygotes show a significant expansion of CD62L+ naive T cells in blood and bone marrow relative to wild-type controls   (MGI Ref ID J:57976)
    • 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   (MGI Ref ID J:57976)
  • 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)   (MGI Ref ID J:57976)
    • unlike wild-type B cells, mutant B cells rapidly leave the outer PALS after being transferred into wild-type recipients   (MGI Ref ID J:57976)

Ccr7tm1Rfor/Ccr7tm1Rfor

        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   (MGI Ref ID J:134784)
View Research Applications

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

Hematological Research
Immunological Defects
      B and T cell deficiency

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

Internal/Organ Research
Lymphoid Tissue Defects
      B and T cell deficiency
      T cell deficiency

Research Tools
Immunology, Inflammation and Autoimmunity Research
      B and T cell deficiency
      B cell deficiency
      T cell deficiency
      genes regulating susceptibility to infectious disease and endotoxin

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ccr7tm1Rfor
Allele Name targeted mutation 1, Reinhold Forster
Allele Type Targeted (Null/Knockout)
Common Name(s) CCR7-;
Mutation Made By Martin Lipp,   Max-Delbrueck-Center
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14K
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Ccr7, chemokine (C-C motif) receptor 7
Chromosome 11
Gene Common Name(s) BLR2; CC-CKR-7; CCR-7; CD197; CDw197; CMKBR7; Cmkbr7; EBI1; Ebi1h; Epstein-Barr virus induced gene 1 homolog; chemokine (C-C) receptor 7;
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. [MGI Ref ID J:57976]

Genotyping

Genotyping Information

Genotyping Protocols

Ccr7suptm1Rfor,

SEPARATED MELT



Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

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):23-33. [PubMed: 10520991]  [MGI Ref ID J:57976]

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):461-70. [PubMed: 14768051]  [MGI Ref ID J:121522]

Additional References

Ccr7tm1Rfor related

Achtman AH; Hopken UE; Bernert C; Lipp M. 2009. CCR7-deficient mice develop atypically persistent germinal centers in response to thymus-independent type 2 antigens. J Leukoc Biol 85(3):409-17. [PubMed: 19074554]  [MGI Ref ID J:146058]

Anderson BE; Taylor PA; McNiff JM; Jain D; Demetris AJ; Panoskaltsis-Mortari A; Ager A; Blazar BR; Shlomchik WD; Shlomchik MJ. 2008. Effects of donor T-cell trafficking and priming site on graft-versus-host disease induction by naive and memory phenotype CD4 T cells. Blood 111(10):5242-51. [PubMed: 18285547]  [MGI Ref ID J:135662]

Asperti-Boursin F; Real E; Bismuth G; Trautmann A; Donnadieu E. 2007. CCR7 ligands control basal T cell motility within lymph node slices in a phosphoinositide 3-kinase-independent manner. J Exp Med 204(5):1167-79. [PubMed: 17485513]  [MGI Ref ID J:125717]

Azukizawa H; Dohler A; Kanazawa N; Nayak A; Lipp M; Malissen B; Autenrieth I; Katayama I; Riemann M; Weih F; Berberich-Siebelt F; Lutz MB. 2011. Steady state migratory RelB+ langerin+ dermal dendritic cells mediate peripheral induction of antigen-specific CD4+ CD25+ Foxp3+ regulatory T cells. Eur J Immunol 41(5):1420-34. [PubMed: 21469094]  [MGI Ref ID J:175408]

Bakocevic N; Worbs T; Davalos-Misslitz A; Forster R. 2010. T cell-dendritic cell interaction dynamics during the induction of respiratory tolerance and immunity. J Immunol 184(3):1317-27. [PubMed: 20042584]  [MGI Ref ID J:159503]

Bao X; Moseman EA; Saito H; Petryanik B; Thiriot A; Hatakeyama S; Ito Y; Kawashima H; Yamaguchi Y; Lowe JB; von Andrian UH; Fukuda M. 2010. Endothelial heparan sulfate controls chemokine presentation in recruitment of lymphocytes and dendritic cells to lymph nodes. Immunity 33(5):817-29. [PubMed: 21093315]  [MGI Ref ID J:167007]

Beauvillain C; Cunin P; Doni A; Scotet M; Jaillon S; Loiry ML; Magistrelli G; Masternak K; Chevailler A; Delneste Y; Jeannin P. 2011. CCR7 is involved in the migration of neutrophils to lymph nodes. Blood 117(4):1196-204. [PubMed: 21051556]  [MGI Ref ID J:168511]

Benahmed F; Chyou S; Dasoveanu D; Chen J; Kumar V; Iwakura Y; Lu TT. 2014. Multiple CD11c+ cells collaboratively express IL-1beta to modulate stromal vascular endothelial growth factor and lymph node vascular-stromal growth. J Immunol 192(9):4153-63. [PubMed: 24659690]  [MGI Ref ID J:209986]

Bessa J; Jegerlehner A; Hinton HJ; Pumpens P; Saudan P; Schneider P; Bachmann MF. 2009. Alveolar macrophages and lung dendritic cells sense RNA and drive mucosal IgA responses. J Immunol 183(6):3788-99. [PubMed: 19710454]  [MGI Ref ID J:152307]

Braun A; Worbs T; Moschovakis GL; Halle S; Hoffmann K; Bolter J; Munk A; Forster R. 2011. Afferent lymph-derived T cells and DCs use different chemokine receptor CCR7-dependent routes for entry into the lymph node and intranodal migration. Nat Immunol 12(9):879-87. [PubMed: 21841786]  [MGI Ref ID J:176463]

Britschgi MR; Link A; Lissandrin TK; Luther SA. 2008. Dynamic modulation of CCR7 expression and function on naive T lymphocytes in vivo. J Immunol 181(11):7681-8. [PubMed: 19017956]  [MGI Ref ID J:142197]

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Brown MN; Fintushel SR; Lee MH; Jennrich S; Geherin SA; Hay JB; Butcher EC; Debes GF. 2010. Chemoattractant receptors and lymphocyte egress from extralymphoid tissue: changing requirements during the course of inflammation. J Immunol 185(8):4873-82. [PubMed: 20833836]  [MGI Ref ID J:164737]

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Platt AM; Rutkowski JM; Martel C; Kuan EL; Ivanov S; Swartz MA; Randolph GJ. 2013. Normal Dendritic Cell Mobilization to Lymph Nodes under Conditions of Severe Lymphatic Hypoplasia. J Immunol 190(9):4608-20. [PubMed: 23530147]  [MGI Ref ID J:195520]

Rappert A; Biber K; Nolte C; Lipp M; Schubel A; Lu B; Gerard NP; Gerard C; Boddeke HW; Kettenmann H. 2002. Secondary lymphoid tissue chemokine (CCL21) activates CXCR3 to trigger a Cl(-) current and chemotaxis in murine microglia. J Immunol 168(7):3221-6. [PubMed: 11907075]  [MGI Ref ID J:75583]

Reboldi A; Coisne C; Baumjohann D; Benvenuto F; Bottinelli D; Lira S; Uccelli A; Lanzavecchia A; Engelhardt B; Sallusto F. 2009. C-C chemokine receptor 6-regulated entry of TH-17 cells into the CNS through the choroid plexus is required for the initiation of EAE. Nat Immunol 10(5):514-23. [PubMed: 19305396]  [MGI Ref ID J:148286]

Rehm A; Mensen A; Schradi K; Gerlach K; Wittstock S; Winter S; Buchner G; Dorken B; Lipp M; Hopken UE. 2011. Cooperative function of CCR7 and lymphotoxin in the formation of a lymphoma-permissive niche within murine secondary lymphoid organs. Blood 118(4):1020-33. [PubMed: 21586747]  [MGI Ref ID J:174881]

Ripen AM; Nitta T; Murata S; Tanaka K; Takahama Y. 2011. Ontogeny of thymic cortical epithelial cells expressing the thymoproteasome subunit beta5t. Eur J Immunol 41(5):1278-87. [PubMed: 21469133]  [MGI Ref ID J:175402]

Sakai N; Wada T; Yokoyama H; Lipp M; Ueha S; Matsushima K; Kaneko S. 2006. Secondary lymphoid tissue chemokine (SLC/CCL21)/CCR7 signaling regulates fibrocytes in renal fibrosis. Proc Natl Acad Sci U S A 103(38):14098-103. [PubMed: 16966615]  [MGI Ref ID J:113652]

Satpathy AT; Briseno CG; Lee JS; Ng D; Manieri NA; Kc W; Wu X; Thomas SR; Lee WL; Turkoz M; McDonald KG; Meredith MM; Song C; Guidos CJ; Newberry RD; Ouyang W; Murphy TL; Stappenbeck TS; Gommerman JL; Nussenzweig MC; Colonna M; Kopan R; Murphy KM. 2013. Notch2-dependent classical dendritic cells orchestrate intestinal immunity to attaching-and-effacing bacterial pathogens. Nat Immunol 14(9):937-48. [PubMed: 23913046]  [MGI Ref ID J:208234]

Schmid MA; Takizawa H; Baumjohann DR; Saito Y; Manz MG. 2011. Bone marrow dendritic cell progenitors sense pathogens via Toll-like receptors and subsequently migrate to inflamed lymph nodes. Blood 118(18):4829-40. [PubMed: 21908421]  [MGI Ref ID J:178795]

Schneider MA; Meingassner JG; Lipp M; Moore HD; Rot A. 2007. CCR7 is required for the in vivo function of CD4+ CD25+ regulatory T cells. J Exp Med 204(4):735-45. [PubMed: 17371928]  [MGI Ref ID J:125597]

Schulz O; Jaensson E; Persson EK; Liu X; Worbs T; Agace WW; Pabst O. 2009. Intestinal CD103+, but not CX3CR1+, antigen sampling cells migrate in lymph and serve classical dendritic cell functions. J Exp Med 206(13):3101-14. [PubMed: 20008524]  [MGI Ref ID J:155671]

Schumann K; Lammermann T; Bruckner M; Legler DF; Polleux J; Spatz JP; Schuler G; Forster R; Lutz MB; Sorokin L; Sixt M. 2010. Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells. Immunity 32(5):703-13. [PubMed: 20471289]  [MGI Ref ID J:160695]

Seo KY; Han SJ; Cha HR; Seo SU; Song JH; Chung SH; Kweon MN. 2010. Eye mucosa: an efficient vaccine delivery route for inducing protective immunity. J Immunol 185(6):3610-9. [PubMed: 20709955]  [MGI Ref ID J:163825]

Seth S; Oberdorfer L; Hyde R; Hoff K; Thies V; Worbs T; Schmitz S; Forster R. 2011. CCR7 Essentially Contributes to the Homing of Plasmacytoid Dendritic Cells to Lymph Nodes under Steady-State As Well As Inflammatory Conditions. J Immunol 186(6):3364-72. [PubMed: 21296980]  [MGI Ref ID J:169774]

Shannon LA; McBurney TM; Wells MA; Roth ME; Calloway PA; Bill CA; Islam S; Vines CM. 2012. CCR7/CCL19 controls expression of EDG-1 in T cells. J Biol Chem 287(15):11656-64. [PubMed: 22334704]  [MGI Ref ID J:211764]

Shields JD; Kourtis IC; Tomei AA; Roberts JM; Swartz MA. 2010. Induction of lymphoidlike stroma and immune escape by tumors that express the chemokine CCL21. Science 328(5979):749-52. [PubMed: 20339029]  [MGI Ref ID J:159521]

Smigiel KS; Richards E; Srivastava S; Thomas KR; Dudda JC; Klonowski KD; Campbell DJ. 2014. CCR7 provides localized access to IL-2 and defines homeostatically distinct regulatory T cell subsets. J Exp Med 211(1):121-36. [PubMed: 24378538]  [MGI Ref ID J:208352]

Tamoutounour S; Guilliams M; Montanana Sanchis F; Liu H; Terhorst D; Malosse C; Pollet E; Ardouin L; Luche H; Sanchez C; Dalod M; Malissen B; Henri S. 2013. Origins and functional specialization of macrophages and of conventional and monocyte-derived dendritic cells in mouse skin. Immunity 39(5):925-38. [PubMed: 24184057]  [MGI Ref ID J:209012]

Tamoutounour S; Henri S; Lelouard H; de Bovis B; de Haar C; van der Woude CJ; Woltman AM; Reyal Y; Bonnet D; Sichien D; Bain CC; Mowat AM; Reis E Sousa C; Poulin LF; Malissen B; Guilliams M. 2012. CD64 distinguishes macrophages from dendritic cells in the gut and reveals the Th1-inducing role of mesenteric lymph node macrophages during colitis. Eur J Immunol 42(12):3150-66. [PubMed: 22936024]  [MGI Ref ID J:190343]

Ueha S; Yoneyama H; Hontsu S; Kurachi M; Kitabatake M; Abe J; Yoshie O; Shibayama S; Sugiyama T; Matsushima K. 2007. CCR7 mediates the migration of Foxp3+ regulatory T cells to the paracortical areas of peripheral lymph nodes through high endothelial venules. J Leukoc Biol 82(5):1230-8. [PubMed: 17698914]  [MGI Ref ID J:127181]

Ueno T; Hara K; Willis MS; Malin MA; Hopken UE; Gray DH; Matsushima K; Lipp M; Springer TA; Boyd RL; Yoshie O; Takahama Y. 2002. Role for CCR7 ligands in the emigration of newly generated T lymphocytes from the neonatal thymus. Immunity 16(2):205-18. [PubMed: 11869682]  [MGI Ref ID J:113513]

Ueno T; Saito F; Gray DH; Kuse S; Hieshima K; Nakano H; Kakiuchi T; Lipp M; Boyd RL; Takahama Y. 2004. CCR7 signals are essential for cortex-medulla migration of developing thymocytes. J Exp Med 200(4):493-505. [PubMed: 15302902]  [MGI Ref ID J:93960]

Umemoto E; Otani K; Ikeno T; Verjan Garcia N; Hayasaka H; Bai Z; Jang MH; Tanaka T; Nagasawa T; Ueda K; Miyasaka M. 2012. Constitutive plasmacytoid dendritic cell migration to the splenic white pulp is cooperatively regulated by CCR7- and CXCR4-mediated signaling. J Immunol 189(1):191-9. [PubMed: 22634622]  [MGI Ref ID J:188949]

Unsoeld H; Krautwald S; Voehringer D; Kunzendorf U; Pircher H. 2002. Cutting edge: CCR7+ and CCR7- memory T cells do not differ in immediate effector cell function. J Immunol 169(2):638-41. [PubMed: 12097363]  [MGI Ref ID J:123839]

Vander Lugt B; Tubo NJ; Nizza ST; Boes M; Malissen B; Fuhlbrigge RC; Kupper TS; Campbell JJ. 2013. CCR7 plays no appreciable role in trafficking of central memory CD4 T cells to lymph nodes. J Immunol 191(6):3119-27. [PubMed: 23935190]  [MGI Ref ID J:205784]

Vigl B; Aebischer D; Nitschke M; Iolyeva M; Rothlin T; Antsiferova O; Halin C. 2011. Tissue inflammation modulates gene expression of lymphatic endothelial cells and dendritic cell migration in a stimulus-dependent manner. Blood 118(1):205-15. [PubMed: 21596851]  [MGI Ref ID J:174878]

Voedisch S; Koenecke C; David S; Herbrand H; Forster R; Rhen M; Pabst O. 2009. Mesenteric lymph nodes confine dendritic cell-mediated dissemination of Salmonella enterica serovar Typhimurium and limit systemic disease in mice. Infect Immun 77(8):3170-80. [PubMed: 19506012]  [MGI Ref ID J:151418]

Wan W; Lionakis MS; Liu Q; Roffe E; Murphy PM. 2013. Genetic deletion of chemokine receptor Ccr7 exacerbates atherogenesis in ApoE-deficient mice. Cardiovasc Res 97(3):580-8. [PubMed: 23180724]  [MGI Ref ID J:210283]

Wendland M; Willenzon S; Kocks J; Davalos-Misslitz AC; Hammerschmidt SI; Schumann K; Kremmer E; Sixt M; Hoffmeyer A; Pabst O; Forster R. 2011. Lymph node T cell homeostasis relies on steady state homing of dendritic cells. Immunity 35(6):945-57. [PubMed: 22195748]  [MGI Ref ID J:179277]

Winau F; Weber S; Sad S; de Diego J; Hoops SL; Breiden B; Sandhoff K; Brinkmann V; Kaufmann SH; Schaible UE. 2006. Apoptotic vesicles crossprime CD8 T cells and protect against tuberculosis. Immunity 24(1):105-17. [PubMed: 16413927]  [MGI Ref ID J:113317]

Winter S; Rehm A; Wichner K; Scheel T; Batra A; Siegmund B; Berek C; Lipp M; Hopken UE. 2011. Manifestation of Spontaneous and Early Autoimmune Gastritis in CCR7-Deficient Mice. Am J Pathol 179(2):754-65. [PubMed: 21801869]  [MGI Ref ID J:174601]

Worbs T; Mempel TR; Bolter J; von Andrian UH; Forster R. 2007. CCR7 ligands stimulate the intranodal motility of T lymphocytes in vivo. J Exp Med 204(3):489-95. [PubMed: 17325198]  [MGI Ref ID J:125363]

Yasuda T; Kuwabara T; Nakano H; Aritomi K; Onodera T; Lipp M; Takahama Y; Kakiuchi T. 2007. Chemokines CCL19 and CCL21 promote activation-induced cell death of antigen-responding T cells. Blood 109(2):449-56. [PubMed: 16973962]  [MGI Ref ID J:144008]

Yoshino M; Okuyama K; Murata A; Tomura M; Hayashi S. 2012. CCR7-independent transport of skin antigens occurs in the dermis. Eur J Immunol 42(6):1459-67. [PubMed: 22622847]  [MGI Ref ID J:187762]

Zhang N; Schroppel B; Lal G; Jakubzick C; Mao X; Chen D; Yin N; Jessberger R; Ochando JC; Ding Y; Bromberg JS. 2009. Regulatory T cells sequentially migrate from inflamed tissues to draining lymph nodes to suppress the alloimmune response. Immunity 30(3):458-69. [PubMed: 19303390]  [MGI Ref ID J:147032]

Zhao C; Wood MW; Galyov EE; Hopken UE; Lipp M; Bodmer HC; Tough DF; Carter RW. 2006. Salmonella typhimurium infection triggers dendritic cells and macrophages to adopt distinct migration patterns in vivo. Eur J Immunol 36(11):2939-50. [PubMed: 17048271]  [MGI Ref ID J:117000]

Ziegler E; Oberbarnscheidt M; Bulfone-Paus S; Forster R; Kunzendorf U; Krautwald S. 2007. CCR7 signaling inhibits T cell proliferation. J Immunol 179(10):6485-93. [PubMed: 17982037]  [MGI Ref ID J:153869]

del Rio ML; Rodriguez-Barbosa JI; Kremmer E; Forster R. 2007. CD103- and CD103+ bronchial lymph node dendritic cells are specialized in presenting and cross-presenting innocuous antigen to CD4+ and CD8+ T cells. J Immunol 178(11):6861-6. [PubMed: 17513734]  [MGI Ref ID J:147845]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, homozygous mice are bred.
Mating SystemHomozygote x Homozygote         (Female x Male)   15-DEC-07
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHomozygous for Ccr7tm1Rfor  
Price per Pair (US dollars $)Pair Genotype
$399.80Homozygous for Ccr7tm1Rfor x Homozygous for Ccr7tm1Rfor  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHomozygous for Ccr7tm1Rfor  
Price per Pair (US dollars $)Pair Genotype
$519.80Homozygous for Ccr7tm1Rfor x Homozygous for Ccr7tm1Rfor  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Control Information

  Control
   000664 C57BL/6J (approximate)
   005304 C57BL/6NJ (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice
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Tel: 1-800-422-6423 or 1-207-288-5845
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

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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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