Strain Name:

C.129(B6)-Tlr2tm1Kir/J

Stock Number:

022507

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Availability:

Cryopreserved - Ready for recovery

This Tlr2 knockout strain is useful in studies of mucosal immune responses and host response to bacterial endotoxins.

Description

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

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
 
Donating Investigator Terry D. Connell,   University of Buffalo

Description
The toll-like receptor 2 protein, TLR2, which is expressed predominantly in peripheral blood leukocytes, plays a critical role in pathogen recognition and activation of innate immunity. Specifically, TLR2 mediates host response to Gram-positive bacteria and yeast via stimulation of NF-kappaB. Mice that are homozygous for this targeted mutation of the Tlr2 gene are viable and fertile. No gene product (protein) is detected by Western blot analysis of isolated peritoneal macrophages. Bone marrow derived macrophages from homozygotes on the congenic C57BL/6 background do not respond to spirochete (Borrelia burgdorferi) lipoprotein challenge, although non-lipoprotein sonicate stimulates activation. Arthritis due to B. burgdorferi infection, as assessed by rear ankle swelling, is more severe in mutant mice on the congenic C57BL/6 background. Tissues of infected B6 congenic mutants can contain up to 100 times higher bacteria levels than those found in wildtype littermates. Elevated spirochete numbers persist 8 weeks post-infection. Homozygotes on the congenic C57BL/6 background do not produce TNF-alpha or IL-6, and do not develop symptoms of illness when treated with leptospiral (Leptospira interrogans) lippolysaccharide (LPS). Homozygotes on the congenic BALB/c background display reduced dendritic cell recruitment into NALT (nasal-associated lymphoid tissue) and cervical lymph node tissue in response to antigen challenge. In comparison to wildtype BALB/c mice, homozygotes on the congenic BALB/c background do not respond to TLR2 agonists in respect to antigen uptake and expression of CCR7 by dendritic cells. Likewise, in response to antigen challenge, homozygotes on the congenic BALB/c background exhibit reduced antigen-specific CD4 T cell proliferation and dendritic cell recruitment into NALT (nasal-associated lymphoid tissue) and cervical lymph node tissue when compared to those responses in wildtype BALB/c mice.

Development
A targeting vector, designed by Dr. Carsten J. Kirschning (Technical University of Munich), containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt sequence of the targeted gene encoding the C-terminus of the extracellular and part of the transmembrane domains. The construct was electroporated into 129/SvJ derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Heterozygotes were intercrossed, and then backcrossed to C57BL/6J for 9 generations. Dr. Terry D. Connell (University of Buffalo) then backcrossed the mice to BALB/cAnNHsd for 7 generations using a speed congenic protocol. Upon arrival at The Jackson Laboratory, the mice were crossed to BALB/cByJ (Stock No. 001026) at least once to establish the colony.

Control Information

  Control
   Wild-type from the colony
   001026 BALB/cByJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Tlr2tm1Kir allele
004650   B6.129-Tlr2tm1Kir/J
View Strains carrying   Tlr2tm1Kir     (1 strain)

Strains carrying other alleles of Tlr2
005846   B6.129S1-Tlr2tm1Dgen/J
View Strains carrying other alleles of Tlr2     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Leprosy, Susceptibility to, 3; LPRS3   (TLR2)
Mycobacterium Tuberculosis, Susceptibility to   (TLR2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Tlr2tm1Kir/Tlr2tm1Kir

        either: (involves: 129/Sv * C57BL/6) or (involves: 129/Sv * C57BL/6 * C57BL/6J)
  • immune system phenotype
  • abnormal innate immunity
    • homozygotes exhibit an abnormal innate host defense to infection with Borrelia burgdorferi, as shown by a failure to control spirochete levels in infected tissues   (MGI Ref ID J:85323)
    • in contrast, homozygotes develop normal Borrelia-specific Ab responses, indicating that acquired host defense is unimpaired   (MGI Ref ID J:85323)
    • abnormal macrophage physiology
      • in vitro, mutant BMDMs do not respond to 500 ng/ml of B. burgdorferi recombinant OspA, as shown by a failure to elicit IL-6, IL-10, TNF and nitrate production relative to BMDMs from control C3H/HeN and C57BL/6 mice   (MGI Ref ID J:85323)
      • mutant BMDMs fail to respond to 5 um/ml OspA (a 10-fold higher concentration), as shown by a severely diminished production of nitrate, IL-6, IL-10, and TNF relative to wild-type BMDMs   (MGI Ref ID J:85323)
      • mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs   (MGI Ref ID J:85323)
      • however, mutant BMDMs do show a strong response to repurified LPS (100 ng/ml)   (MGI Ref ID J:85323)
      • decreased macrophage cytokine production
        • TNF secretion by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
        • TNF secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
      • decreased macrophage nitric oxide production
        • NO production by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
        • NO production by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
        • mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs   (MGI Ref ID J:85323)
  • decreased interleukin-10 secretion
    • IL-10 secretion by mutant bone marrow-derived macrophages (BMDMs) is abolished in response to 500 ng/ml of B. burgdorferi recombinant outer surface protein A (OspA)   (MGI Ref ID J:85323)
    • IL-10 secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
  • decreased interleukin-6 secretion
    • IL-6 secretion by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
    • IL-6 secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
  • increased susceptibility to bacterial infection
    • at 4 weeks postinfection with 2 x 103 organisms of B. burgdorferi (N40 isolate), homozygotes exhibit a striking increase in rear ankle swelling relative to wild-type and heterozygous controls, with both rear ankle joints showing uniformly increased edema; however, individual disease parameters and overall arthritic lesion severity is not significantly different between similarly-infected mutant and control mice   (MGI Ref ID J:85323)
    • at 2 and 4 weeks postinfection, all homozygotes harbor up to 100-fold more B. burgdorferi spirochetes in heart, rear ankle joints, and ears than wild-type and heterozygous controls   (MGI Ref ID J:85323)
    • at 2 weeks postinfection, homozygotes harbor up ~7-fold more B. burgdorferi spirochetes in spleen than wild-type controls   (MGI Ref ID J:85323)
    • in homozygotes, extremely high spirochete levels of B. burgdorferi persist in infected hearts, rear ankles, and ears at 8 weeks postinfection   (MGI Ref ID J:85323)
    • however, homozygotes display a normal acquired humoral response to B. burgdorferi infection, as measured by quantity of Borrelia-specific Ig isotypes, the kinetics of class switching to IgG, and the complexity of the antigens recognized   (MGI Ref ID J:85323)
  • homeostasis/metabolism phenotype
  • decreased macrophage nitric oxide production
    • NO production by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
    • NO production by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
    • mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs   (MGI Ref ID J:85323)
  • hematopoietic system phenotype
  • abnormal macrophage physiology
    • in vitro, mutant BMDMs do not respond to 500 ng/ml of B. burgdorferi recombinant OspA, as shown by a failure to elicit IL-6, IL-10, TNF and nitrate production relative to BMDMs from control C3H/HeN and C57BL/6 mice   (MGI Ref ID J:85323)
    • mutant BMDMs fail to respond to 5 um/ml OspA (a 10-fold higher concentration), as shown by a severely diminished production of nitrate, IL-6, IL-10, and TNF relative to wild-type BMDMs   (MGI Ref ID J:85323)
    • mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs   (MGI Ref ID J:85323)
    • however, mutant BMDMs do show a strong response to repurified LPS (100 ng/ml)   (MGI Ref ID J:85323)
    • decreased macrophage cytokine production
      • TNF secretion by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
      • TNF secretion by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
    • decreased macrophage nitric oxide production
      • NO production by mutant BMDMs is abolished in response to 500 ng/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
      • NO production by mutant BMDMs is severely reduced in response to 5 ug/ml of B. burgdorferi OspA   (MGI Ref ID J:85323)
      • mutant BMDMs do respond to nonlipoprotein components of sonicated B. burgdorferi (N40) spirochetes, but require 10- to 100-fold more sonicate for equivalent nitrate production as wild-type BMDMs   (MGI Ref ID J:85323)

Tlr2tm1Kir/Tlr2tm1Kir

        Background Not Specified
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • homozygous null mice succumbed to S. aureus infection within 5 days   (MGI Ref ID J:96018)
  • immune system phenotype
  • abnormal macrophage physiology
    • peritoneal macrophages were completely unresponsive and produced little or no TNF when stimulated with lipoteichoic acid (LTA) or macrophage-activating lipopeptide 2 (MALP-2) from Mycoplasma pneumoniae   (MGI Ref ID J:96018)
  • increased susceptibility to bacterial infection
    • during a 7-dap period, homozygous null mice were permissive for the growth of intradermally inoculated S. aureus, whereas the bacteria were cleared from wildtype   (MGI Ref ID J:96018)
  • hematopoietic system phenotype
  • abnormal macrophage physiology
    • peritoneal macrophages were completely unresponsive and produced little or no TNF when stimulated with lipoteichoic acid (LTA) or macrophage-activating lipopeptide 2 (MALP-2) from Mycoplasma pneumoniae   (MGI Ref ID J:96018)

Tlr2tm1Kir/Tlr2tm1Kir

        B6.129-Tlr2tm1Kir
  • mortality/aging
  • decreased susceptibility to bacterial infection induced morbidity/mortality
    • mutants are protected from bacterial lipoteichoic acid exposure after priming by IFNG and sensitization with D-galactosamine, while Tlr4-deficient mice and wild-type are susceptible to lethal shock by this treatment   (MGI Ref ID J:121930)
    • heat-inactivated E. coli exposure results in fatal toxemia however, similar to wild-type mice heat-inactivated E. coli exposure results in fatal toxemia   (MGI Ref ID J:121930)
    • susceptibilities to L. monocytogenes and S. aureus challenge are not different from wild-type mice   (MGI Ref ID J:121930)
  • premature death   (MGI Ref ID J:165105)
    • 60% mortality due to weight loss resulting from induced colonic inflammation   (MGI Ref ID J:128329)
  • immune system phenotype
  • abnormal cellular extravasation
    • accumulation of monocyte/macrophage in surrounding tissues is significantly reduced relative to controls after femoral artery ligation   (MGI Ref ID J:171028)
  • abnormal cytokine secretion
    • systemic challenge with Pam3-CSK4, a bacterial lipopeptide analog, does not induce substantial secretion of Il6 or TNFalpha, compared to marked levels produced in wild-type mice   (MGI Ref ID J:121930)
    • decreased interleukin-1 beta secretion
      • IL1-beta secretion by peritoneal macrophages is reduced by 50% in response to Listeria infection   (MGI Ref ID J:129871)
      • peritoneal macrophages fail to secrete IL-1beta in response to a TLR2 agonist   (MGI Ref ID J:129871)
    • decreased interleukin-6 secretion
      • IL-6 secretion by peritoneal macrophages is reduced by 8-fold in response to Listeria infection   (MGI Ref ID J:129871)
      • peritoneal macrophages fail to secrete IL6 in response to a TLR2 agonist   (MGI Ref ID J:129871)
    • decreased tumor necrosis factor secretion
      • TNF secretion by peritoneal macrophages is reduced by 50% in response to Listeria infection   (MGI Ref ID J:129871)
  • decreased circulating tumor necrosis factor level
    • in females on high fat diet at 20 weeks   (MGI Ref ID J:162168)
    • also reduced MCP-1 levels in females on high fat diet at 20 weeks   (MGI Ref ID J:162168)
  • decreased splenocyte proliferation
    • splenocytes do not proliferate in response to bacterial peptidoglycan or lipoteichoic acid, but do respond normally with proliferation to enterobacterial LPS   (MGI Ref ID J:121930)
  • decreased susceptibility to bacterial infection induced morbidity/mortality
    • mutants are protected from bacterial lipoteichoic acid exposure after priming by IFNG and sensitization with D-galactosamine, while Tlr4-deficient mice and wild-type are susceptible to lethal shock by this treatment   (MGI Ref ID J:121930)
    • heat-inactivated E. coli exposure results in fatal toxemia however, similar to wild-type mice heat-inactivated E. coli exposure results in fatal toxemia   (MGI Ref ID J:121930)
    • susceptibilities to L. monocytogenes and S. aureus challenge are not different from wild-type mice   (MGI Ref ID J:121930)
  • increased susceptibility to induced colitis
    • inflammation level significantly greater 14 days into procedure to induce colitis   (MGI Ref ID J:165105)
  • cellular phenotype
  • abnormal cellular extravasation
    • accumulation of monocyte/macrophage in surrounding tissues is significantly reduced relative to controls after femoral artery ligation   (MGI Ref ID J:171028)
  • decreased neuron apoptosis
    • neurons are resistant to apoptosis caused by glucose deficiency   (MGI Ref ID J:124100)
  • decreased splenocyte proliferation
    • splenocytes do not proliferate in response to bacterial peptidoglycan or lipoteichoic acid, but do respond normally with proliferation to enterobacterial LPS   (MGI Ref ID J:121930)
  • nervous system phenotype
  • CNS ischemia
    • increased mortality occurring within 24 hours due to ischemia/reperfusion   (MGI Ref ID J:148091)
    • reduced neurological score after ischemia/reperfusion   (MGI Ref ID J:148091)
    • increased infarct size at 24 hours after ischemia/reperfusion   (MGI Ref ID J:148091)
    • large areas of pan-necrosis in the distribution area of the middle cerebral artery   (MGI Ref ID J:148091)
  • decreased cerebral infarction size
    • damage due to middle cerebral artery occlusion is considerably reduced   (MGI Ref ID J:124100)
  • decreased neuron apoptosis
    • neurons are resistant to apoptosis caused by glucose deficiency   (MGI Ref ID J:124100)
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis   (MGI Ref ID J:162168)
    • decreased circulating insulin level
      • fasting circulating insulin levels are reduced at both 12 and 20 weeks on a high fat diet   (MGI Ref ID J:162168)
    • improved glucose tolerance
      • improved glucose tolerance in females after 12 weeks on a high fat diet relative to controls   (MGI Ref ID J:162168)
      • glucose homeostasis on a normal diet is similar to controls   (MGI Ref ID J:162168)
    • increased insulin secretion
      • beta cell insulin secretion in response to glucose challenge is markedly improved in females relative to controls at 20 weeks   (MGI Ref ID J:162168)
    • increased insulin sensitivity
      • insulin sensitivity in response to glucose challenge is markedly improved in females relative to controls at 20 weeks   (MGI Ref ID J:162168)
      • liver insulin sensitivity is preserved after 20 weeks on a high fat diet   (MGI Ref ID J:162168)
      • reduced hepatic glucose production in a hyperinsulinaemic clamp   (MGI Ref ID J:162168)
      • males also show increased insulin sensitivity   (MGI Ref ID J:162168)
  • decreased cerebral infarction size
    • damage due to middle cerebral artery occlusion is considerably reduced   (MGI Ref ID J:124100)
  • decreased circulating leptin level
    • in females on a high fat diet at 20 weeks   (MGI Ref ID J:162168)
  • decreased circulating tumor necrosis factor level
    • in females on high fat diet at 20 weeks   (MGI Ref ID J:162168)
    • also reduced MCP-1 levels in females on high fat diet at 20 weeks   (MGI Ref ID J:162168)
  • decreased susceptibility to kidney reperfusion injury
    • significantly protected from ischemia reperfusion injury as measured by serum creatinine levels 24 hours after injury   (MGI Ref ID J:146120)
  • increased energy expenditure
    • in females on high fat diet   (MGI Ref ID J:162168)
    • preferential use of lipids as an energy source   (MGI Ref ID J:162168)
  • adipose tissue phenotype
  • abnormal adipocyte glucose uptake
    • improved insulin stimulated glucose uptake in females on a high fat diet   (MGI Ref ID J:162168)
  • abnormal fat pad morphology
    • reduced perigonadal fat pad weight in females on a high fat diet   (MGI Ref ID J:162168)
  • decreased fat cell size
    • adipocytes are smaller in females on a high fat diet   (MGI Ref ID J:162168)
  • behavior/neurological phenotype
  • increased food intake
    • increased calorie consumption in females on a high fat diet   (MGI Ref ID J:162168)
  • liver/biliary system phenotype
  • decreased susceptibility to hepatic steatosis
    • reduced lipid content of the liver   (MGI Ref ID J:162168)
  • cardiovascular system phenotype
  • decreased angiogenesis
    • perfusion restoration is significantly reduced 7 days after femoral artery ligation   (MGI Ref ID J:171028)
  • rectal hemorrhage   (MGI Ref ID J:165105)
    • gross rectal bleeding 5 days after induction of colonic inflammation with dextran sodium sulfate   (MGI Ref ID J:128329)
  • digestive/alimentary phenotype
  • abnormal intestinal epithelium morphology
    • reduced proliferation and increased apoptosis before experimental manipulation   (MGI Ref ID J:165105)
    • abnormal enterocyte morphology
      • compromised intestinal epithelial tight junction barrier   (MGI Ref ID J:128329)
      • increased number of apoptotic intestinal epithelial cells   (MGI Ref ID J:128329)
    • abnormal large intestine crypts of Lieberkuhn morphology
      • aberrant (preneoplastic) crypt foci   (MGI Ref ID J:165105)
      • reduced apoptosis   (MGI Ref ID J:165105)
  • colonic necrosis
    • less necrosis in colon than for controls 14 days after beginning procedure to induce colitis   (MGI Ref ID J:165105)
  • increased susceptibility to induced colitis
    • inflammation level significantly greater 14 days into procedure to induce colitis   (MGI Ref ID J:165105)
  • rectal hemorrhage   (MGI Ref ID J:165105)
    • gross rectal bleeding 5 days after induction of colonic inflammation with dextran sodium sulfate   (MGI Ref ID J:128329)
  • growth/size/body phenotype
  • weight loss   (MGI Ref ID J:165105)
    • severe weight loss as a result of induced colonic inflammation   (MGI Ref ID J:128329)
  • renal/urinary system phenotype
  • decreased susceptibility to kidney reperfusion injury
    • significantly protected from ischemia reperfusion injury as measured by serum creatinine levels 24 hours after injury   (MGI Ref ID J:146120)
  • tumorigenesis
  • increased carcinoma incidence
    • two fold increase in the incidence of carcinomas   (MGI Ref ID J:165105)
  • increased colonic adenoma incidence
    • colorectal adenomas with very distorted glands and an increased level of disorganization   (MGI Ref ID J:165105)
  • increased gastrointestinal tumor incidence
    • tumor burden 2X that of controls   (MGI Ref ID J:165105)
    • particularly in the proximal colon   (MGI Ref ID J:165105)
    • more large tumors   (MGI Ref ID J:165105)
  • endocrine/exocrine gland phenotype
  • abnormal large intestine crypts of Lieberkuhn morphology
    • aberrant (preneoplastic) crypt foci   (MGI Ref ID J:165105)
    • reduced apoptosis   (MGI Ref ID J:165105)
  • increased insulin secretion
    • beta cell insulin secretion in response to glucose challenge is markedly improved in females relative to controls at 20 weeks   (MGI Ref ID J:162168)
  • hematopoietic system phenotype
  • abnormal cellular extravasation
    • accumulation of monocyte/macrophage in surrounding tissues is significantly reduced relative to controls after femoral artery ligation   (MGI Ref ID J:171028)
  • decreased splenocyte proliferation
    • splenocytes do not proliferate in response to bacterial peptidoglycan or lipoteichoic acid, but do respond normally with proliferation to enterobacterial LPS   (MGI Ref ID J:121930)

Tlr2tm1Kir/Tlr2tm1Kir

        involves: 129
  • mortality/aging
  • increased susceptibility to bacterial infection induced morbidity/mortality
    • when infected with Sanger 476, a methicillin-susceptible S. aureus strain, or MW2, a methicillin-resistant S. aureus strain   (MGI Ref ID J:147177)
  • immune system phenotype
  • abnormal interleukin secretion   (MGI Ref ID J:94463)
    • decreased interleukin-1 secretion
      • significantly reduced response to LPS challenge   (MGI Ref ID J:94463)
    • decreased interleukin-6 secretion
      • significantly reduced response to LPS challenge   (MGI Ref ID J:94463)
  • decreased tumor necrosis factor secretion
    • significantly reduced response to LPS challenge   (MGI Ref ID J:94463)
  • increased susceptibility to bacterial infection induced morbidity/mortality
    • when infected with Sanger 476, a methicillin-susceptible S. aureus strain, or MW2, a methicillin-resistant S. aureus strain   (MGI Ref ID J:147177)
  • endocrine/exocrine gland phenotype
  • abnormal adrenal gland morphology   (MGI Ref ID J:94463)
    • abnormal adrenal cortex morphology
      • adrenal gland enlargement primarily involves the cortex   (MGI Ref ID J:94463)
    • enlarged adrenal glands   (MGI Ref ID J:94463)
  • abnormal adrenal gland secretion
    • corticosterone production moderately decreased   (MGI Ref ID J:94463)
  • homeostasis/metabolism phenotype
  • abnormal circulating corticosterone level
    • lipopolysaccharide stimulation results in a smaller increase in plasma glucocorticoid than in controls   (MGI Ref ID J:94463)
    • decreased circulating corticosterone level
      • levels are significantly lower than in controls   (MGI Ref ID J:94463)
      • reduced further after lipoteichoic acid stimulation   (MGI Ref ID J:94463)
  • abnormal circulating pituitary hormone level
    • lipopolysaccharide stimulation results in very little increase in ACTH   (MGI Ref ID J:94463)
    • increased circulating adrenocorticotropin level
      • plasma ACTH is elevated   (MGI Ref ID J:94463)
  • cellular phenotype
  • abnormal endoplasmic reticulum morphology
    • little increase in smooth endoplasmic reticulum or liposome reduction in response to either lipopolysaccharide or lipoteichoic acid stimulation   (MGI Ref ID J:94463)
  • abnormal mitochondrion morphology   (MGI Ref ID J:94463)
    • abnormal mitochondrial shape
      • increased folding of the mitochondrial membrane   (MGI Ref ID J:94463)
    • decreased mitochondria number
      • in adrenocortical cells   (MGI Ref ID J:94463)

Tlr2tm1Kir/Tlr2tm1Kir

        involves: 129 * C57BL/6
  • nervous system phenotype
  • abnormal myelination
    • hyaluronan is unable to block remyelination in the brain of lysolecithin treated homozygotes as it can in controls   (MGI Ref ID J:161285)
View Research Applications

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

Cell Biology Research
Signal Transduction

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
      Tlr deficiency
      genes regulating susceptibility to infectious disease and endotoxin
Immunodeficiency
      Tlr deficiency
Immunodeficiency Associated with Other Defects

Research Tools
Immunology, Inflammation and Autoimmunity Research
      genes regulating susceptibility to infectious disease and endotoxin

Tlr2tm1Kir related

Cell Biology Research
Signal Transduction

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
      Tlr deficiency
      genes regulating susceptibility to infectious disease and endotoxin
Immunodeficiency
      Tlr deficiency
Immunodeficiency Associated with Other Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tlr2tm1Kir
Allele Name targeted mutation 1, Carsten J Kirschning
Allele Type Targeted (Null/Knockout)
Common Name(s) Ly105; TLR2-;
Mutation Made By Carsten Kirschning,   Technical University of Munich
Strain of Origin129
Gene Symbol and Name Tlr2, toll-like receptor 2
Chromosome 3
Gene Common Name(s) CD282; Ly105; TIL4;
Molecular Note Sequence encoding the extracellular domain and a portion of the transmembrane domain was replaced with a neo cassette inserted by homologous recombination. Protein was undetected by Western blot analysis of peritoneal macrophages obtained from homozygousmutant mice. [MGI Ref ID J:130011] [MGI Ref ID J:85323]

Genotyping

Genotyping Information

Genotyping Protocols

Tlr2, High Resolution Melting


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Lee CH; Masso-Welch P; Hajishengallis G; Connell TD. 2011. TLR2-dependent modulation of dendritic cells by LT-IIa-B5, a novel mucosal adjuvant derived from a type II heat-labile enterotoxin. J Leukoc Biol 90(5):911-21. [PubMed: 21791597]  [MGI Ref ID J:178266]

Wooten RM; Ma Y; Yoder RA; Brown JP; Weis JH; Zachary JF; Kirschning CJ; Weis JJ. 2002. Toll-like receptor 2 is required for innate, but not acquired, host defense to Borrelia burgdorferi. J Immunol 168(1):348-55. [PubMed: 11751980]  [MGI Ref ID J:85323]

Additional References

Tlr2tm1Kir related

Abarbanell AM; Wang Y; Herrmann JL; Weil BR; Poynter JA; Manukyan MC; Meldrum DR. 2010. Toll-like receptor 2 mediates mesenchymal stem cell-associated myocardial recovery and VEGF production following acute ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol 298(5):H1529-36. [PubMed: 20173040]  [MGI Ref ID J:159915]

Abe T; Hosur KB; Hajishengallis E; Reis ES; Ricklin D; Lambris JD; Hajishengallis G. 2012. Local complement-targeted intervention in periodontitis: proof-of-concept using a C5a receptor (CD88) antagonist. J Immunol 189(11):5442-8. [PubMed: 23089394]  [MGI Ref ID J:190681]

Amura CR; Renner B; Lyubchenko T; Faubel S; Simonian PL; Thurman JM. 2012. Complement activation and toll-like receptor-2 signaling contribute to cytokine production after renal ischemia/reperfusion. Mol Immunol 52(3-4):249-57. [PubMed: 22750071]  [MGI Ref ID J:188161]

Anand PK; Tait SW; Lamkanfi M; Amer AO; Nunez G; Pages G; Pouyssegur J; McGargill MA; Green DR; Kanneganti TD. 2011. TLR2 and RIP2 Pathways Mediate Autophagy of Listeria monocytogenes via Extracellular Signal-regulated Kinase (ERK) Activation. J Biol Chem 286(50):42981-91. [PubMed: 22033934]  [MGI Ref ID J:178691]

Andrade EB; Alves J; Madureira P; Oliveira L; Ribeiro A; Cordeiro-da-Silva A; Correia-Neves M; Trieu-Cuot P; Ferreira P. 2013. TLR2-induced IL-10 production impairs neutrophil recruitment to infected tissues during neonatal bacterial sepsis. J Immunol 191(9):4759-68. [PubMed: 24078699]  [MGI Ref ID J:206234]

Appledorn DM; Patial S; McBride A; Godbehere S; Van Rooijen N; Parameswaran N; Amalfitano A. 2008. Adenovirus vector-induced innate inflammatory mediators, MAPK signaling, as well as adaptive immune responses are dependent upon both TLR2 and TLR9 in vivo. J Immunol 181(3):2134-44. [PubMed: 18641352]  [MGI Ref ID J:139229]

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Wang Y; Ye F; Ke Q; Wu Q; Yang R; Bu H. 2013. Gender-dependent histone deacetylases injury may contribute to differences in liver recovery rates of male and female mice. Transplant Proc 45(2):463-73. [PubMed: 23498780]  [MGI Ref ID J:198984]

Warger T; Hilf N; Rechtsteiner G; Haselmayer P; Carrick DM; Jonuleit H; von Landenberg P; Rammensee HG; Nicchitta CV; Radsak MP; Schild H. 2006. Interaction of TLR2 and TLR4 ligands with the N-terminal domain of Gp96 amplifies innate and adaptive immune responses. J Biol Chem 281(32):22545-53. [PubMed: 16754684]  [MGI Ref ID J:116459]

Weighardt H; Kaiser-Moore S; Vabulas RM; Kirschning CJ; Wagner H; Holzmann B. 2002. Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection. J Immunol 169(6):2823-7. [PubMed: 12218091]  [MGI Ref ID J:120435]

Werts C; Tapping RI; Mathison JC; Chuang TH; Kravchenko V; Saint Girons I; Haake DA; Godowski PJ; Hayashi F; Ozinsky A; Underhill DM; Kirschning CJ; Wagner H; Aderem A; Tobias PS; Ulevitch RJ. 2001. Leptospiral lipopolysaccharide activates cells through a TLR2-dependent mechanism. Nat Immunol 2(4):346-52. [PubMed: 11276206]  [MGI Ref ID J:130011]

Westwell-Roper C; Dai DL; Soukhatcheva G; Potter KJ; van Rooijen N; Ehses JA; Verchere CB. 2011. IL-1 blockade attenuates islet amyloid polypeptide-induced proinflammatory cytokine release and pancreatic islet graft dysfunction. J Immunol 187(5):2755-65. [PubMed: 21813778]  [MGI Ref ID J:179268]

Winters L; Winters T; Gorup D; Mitrecic D; Curlin M; Kriz J; Gajovic S. 2013. Expression analysis of genes involved in TLR2-related signaling pathway: Inflammation and apoptosis after ischemic brain injury. Neuroscience 238:87-96. [PubMed: 23402853]  [MGI Ref ID J:201370]

Won WJ; Bachmann MF; Kearney JF. 2008. CD36 is differentially expressed on B cell subsets during development and in responses to antigen. J Immunol 180(1):230-7. [PubMed: 18097024]  [MGI Ref ID J:130897]

Wu SC; Yang JC; Rau CS; Chen YC; Lu TH; Lin MW; Tzeng SL; Wu YC; Wu CJ; Hsieh CH. 2013. Profiling circulating microRNA expression in experimental sepsis using cecal ligation and puncture. PLoS One 8(10):e77936. [PubMed: 24205035]  [MGI Ref ID J:209241]

Wu Z; Sawamura T; Kurdowska AK; Ji HL; Idell S; Fu J. 2011. LOX-1 Deletion Improves Neutrophil Responses, Enhances Bacterial Clearance, and Reduces Lung Injury in a Murine Polymicrobial Sepsis Model. Infect Immun 79(7):2865-70. [PubMed: 21576343]  [MGI Ref ID J:173477]

Yang HZ; Cui B; Liu HZ; Chen ZR; Yan HM; Hua F; Hu ZW. 2009. Targeting TLR2 attenuates pulmonary inflammation and fibrosis by reversion of suppressive immune microenvironment. J Immunol 182(1):692-702. [PubMed: 19109203]  [MGI Ref ID J:142877]

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Zeuthen LH; Fink LN; Frokiaer H. 2008. Toll-like receptor 2 and nucleotide-binding oligomerization domain-2 play divergent roles in the recognition of gut-derived lactobacilli and bifidobacteria in dendritic cells. Immunology 124(4):489-502. [PubMed: 18217947]  [MGI Ref ID J:142781]

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Health & husbandry

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

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice can be bred as homozygotes.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

Control Information

  Control
   Wild-type from the colony
   001026 BALB/cByJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

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


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

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

No Warranty

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

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

No Liability

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

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

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

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


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