Overview

Also Known As: CBA/N

CBA/CaHN-Btk^xid/J mice have a mutation in the Bruton's tyrosine kinase gene (Btk), and are a model of human X-linked immunodeficiency. They have a B-lymphocyte-specific defect that results in an inability to launch an antibody response to thymus-independent type II antigens, although they do produce normal amounts of antibody in response to some protein antigens. They have low serum IgM and IgG3 and a reduced number of B-cells. Moreover, the B-cells that are present have a reduced surface IgM to IgD ratio, which suggests a disorder in B-cell maturation.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

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Research Applications

Mouse/Human Gene Homologs
Research Tools
Immunology, Inflammation and Autoimmunity Research

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Base Price

Starting at:

$0.00 Domestic price for male 3-week

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Details

Detailed Description

CBA/CaHN-Btk^xid/J mice have a mutation in the Bruton's tyrosine kinase gene (Btk), and are a model of human X-linked immunodeficiency. They have a B-lymphocyte-specific defect that results in an inability to launch an antibody response to thymus-independent type II antigens, although they do produce normal amounts of antibody in response to some protein antigens. They have low serum IgM and IgG3 and a reduced number of B-cells. Moreover, the B-cells that are present have a reduced surface IgM to IgD ratio, which suggests a disorder in B-cell maturation.

View Flow Cytometry Characterization Data for Immunodeficient JAX Strains

Control Suggestions

Approximate Controls

000654 CBA/CaJ, (The mating scheme, homozygote x hemizygote, does not generate a wild-type control. 000654 may be used as an approximate control whose degree of relationship to CBA/CaHN is uncertain. )

Additional Information

Considerations for Choosing Controls

Selected References

Cancro MP; Sah AP; Levy SL; Allman DM; Schmidt MR; Woodland RT. 2001. xid mice reveal the interplay of homeostasis and Bruton's tyrosine kinase-mediated selection at multiple stages of B cell development. Int Immunol 13(12):1501-14PubMed: 11717191 MGI: J:109858
Amsbaugh DF; Hansen CT; Prescott B; Stashak PW; Barthold DR; Baker PJ. 1972. Genetic control of the antibody response to type 3 pneumococcal polysaccharide in mice. I. Evidence that an X-linked gene plays a decisive role in determining responsiveness. J Exp Med 136(4):931-49PubMed: 4403476 MGI: J:109969
Berning AK; Eicher EM; Paul WE; Scher I. 1980. Mapping of the X-linked immune deficiency mutation (xid) of CBA/N mice. J Immunol 124(4):1875-7PubMed: 7365241 MGI: J:6296

View All References

Genetics

Btk^xid

Allele Symbol: Btk^xid

Allele Name	X linked immune deficiency
Allele Type	Spontaneous
Allele Synonym(s)	X linked immune deficiency; Btk^xid
Gene Symbol and Name	Btk, Bruton agammaglobulinemia tyrosine kinase
Gene Synonym(s)	AT; BPK; AGMX1; xid; X-linked immune deficiency; xid; XLA; ATK; Bruton's tyrosine kinase; AI528679; IMD1; PSCTK1; expressed sequence AI528679; X-linked immune deficiency; IGHD3
Strain of Origin	CBA/HN
Chromosome	X
Molecular Note	The C to T transition point mutation at position 219 is predicted to change amino acid 28 from an arginine to a cysteine in the encoded protein.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Bruton-type agammaglobulinemia

Research Areas By Genotype

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

Genotype: Btk^xid related

Mouse/Human Gene Homologs
- Bruton agammaglobulinemia tyrosine kinase
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - B cell deficiency
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - B cell defects

Mammalian Phenotype Terms by Genotype

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

Genotype: Btk^xid/Btk^xid
involves: CBA/HN * DBA/2N

cellular phenotype

abnormal B cell proliferation
- B cells show response to LPS and poly I:C similar to wild-type cells
- Background Sensitivity - proliferative response in B cells from females is much higher than in cells from female mutants on CBA/HN background

immune system phenotype

abnormal B cell physiology
- spleen cells from unsensitized females cause 3-fold higher chromium release from H-2b antibody treated EL-4 tumor cells than splenocytes from males

abnormal B cell proliferation
- B cells show response to LPS and poly I:C similar to wild-type cells
- Background Sensitivity - proliferative response in B cells from females is much higher than in cells from female mutants on CBA/HN background

decreased B cell number
- Background Sensitivity - numbers are greater in female mutants on CBA * C57BL/6 background (40%) than females on CBA/HN background (22%)
- spleens from females have ~40% immunoglobulin-bearing cells compared to ~50% in controls

spleen hypoplasia
- Background Sensitivity - females on the CBA * DBA/2J (~90 x 10⁶/spleen) have significantly more nucleated spleen cells CBA/HN females (~60 x 10⁶/spleen)
- number of nucleated spleen cells (~90 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

hematopoietic system phenotype

abnormal B cell physiology
- spleen cells from unsensitized females cause 3-fold higher chromium release from H-2b antibody treated EL-4 tumor cells than splenocytes from males

abnormal B cell proliferation
- B cells show response to LPS and poly I:C similar to wild-type cells
- Background Sensitivity - proliferative response in B cells from females is much higher than in cells from female mutants on CBA/HN background

decreased B cell number
- Background Sensitivity - numbers are greater in female mutants on CBA * C57BL/6 background (40%) than females on CBA/HN background (22%)
- spleens from females have ~40% immunoglobulin-bearing cells compared to ~50% in controls

spleen hypoplasia
- Background Sensitivity - females on the CBA * DBA/2J (~90 x 10⁶/spleen) have significantly more nucleated spleen cells CBA/HN females (~60 x 10⁶/spleen)
- number of nucleated spleen cells (~90 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

Genotype: Btk^xid/Y
involves: CBA/HN * DBA/2N

cellular phenotype

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells
- proliferative response occurs slightly later and is much lower in males than in females

hematopoietic system phenotype

decreased B cell number
- spleens have only ~22% immunoglobulin-bearing cells compared to ~50% in controls

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells
- proliferative response occurs slightly later and is much lower in males than in females

spleen hypoplasia
- number of nucleated spleen cells (~50 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

immune system phenotype

decreased B cell number
- spleens have only ~22% immunoglobulin-bearing cells compared to ~50% in controls

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells
- proliferative response occurs slightly later and is much lower in males than in females

spleen hypoplasia
- number of nucleated spleen cells (~50 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

Genotype: Btk^xid/Btk^xid
involves: C57BL/6 * CBA

mammalian phenotype

immune system phenotype
- mucosal-associated invariant T cells (MAIT) that are not found in mice lacking all B cells are found in normal amounts in these mice (i.e. MAIT cells are not dependent on B1 B cells)

Genotype: Btk^xid/?
involves: BALB/c * CBA/N

cellular phenotype

decreased B cell proliferation
- no increase in proliferation is seen after BCR cross-linking

hematopoietic system phenotype

decreased B cell proliferation
- no increase in proliferation is seen after BCR cross-linking

decreased B-1 B cell number
- drastic reduction in the percentage of CD5+B220+ cells in the peritoneum

decreased IgG3 level

decreased IgM level
- basal serum IgM levels are decreased compared to wild-type controls
- serum levels of IgM following TNP-Ficoll treatment are reduced compared to wild-type controls

decreased mature B cell number
- the frequency and number of B cells are reduced in the spleen

immune system phenotype

decreased B cell proliferation
- no increase in proliferation is seen after BCR cross-linking

decreased B-1 B cell number
- drastic reduction in the percentage of CD5+B220+ cells in the peritoneum

decreased IgG3 level

decreased IgM level
- basal serum IgM levels are decreased compared to wild-type controls
- serum levels of IgM following TNP-Ficoll treatment are reduced compared to wild-type controls

decreased mature B cell number
- the frequency and number of B cells are reduced in the spleen

Genotype: Btk^xid/Btk^xid
B6.CBA-Btk

hematopoietic system phenotype

decreased transitional stage B cell number
- CD23+ AA4+ splenic B cell numbers are similar to control
- homozygous female mice exhibit a 2-3 fold decrease in CD23+ AA4+ bone marrow B cells (T2, T3), numbers of CD23- AA4+ cells are consistent with control

immune system phenotype

decreased transitional stage B cell number
- CD23+ AA4+ splenic B cell numbers are similar to control
- homozygous female mice exhibit a 2-3 fold decrease in CD23+ AA4+ bone marrow B cells (T2, T3), numbers of CD23- AA4+ cells are consistent with control

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

Genotype: Btk^xid/Btk^xid
CBA/CaHN-Btk/J

digestive/alimentary phenotype

increased susceptibility to induced colitis
- dextran sulfate sodium-induced colitis results in significant weight loss in wild-type mice by day 10 of DSS treatment while mutants do not exhibit any weight loss at that time

hematopoietic system phenotype

abnormal macrophage physiology
- macrophages (adherent peritoneal exudates cells, PECs) stimulated with LPS show a reduced induction of ROIs than wild-type macrophages at all LPS concentrations

abnormal neutrophil physiology
- mutant polymorphonuclear leukocytes (PMNs) show poorer induction of reactive oxygen intermediates (ROIs) upon LPS stimulation compared to wild-type; NO production is significantly less in mutant PMNs

decreased follicular B cell number
- decrease in IgD^hi IgM^lo mature follicular B cells

decreased neutrophil cell number
- total leukocyte numbers are not significantly altered compared to wild-type, but significantly reduced peripheral PMN frequency in blood is observed in mutants

impaired myelopoiesis
- frequency of monocytic/granulocytic precursors (myeloid CFUs) is significantly reduced compared to wild-type bone marrow
- number of monocytic and granulocytic-lineage cells is significantly reduced in mutant bone marrow

impaired neutrophil phagocytosis
- phagocytic ability of PMNs is somewhat lower, but not significantly, compared to wild-type

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality
- in Salmonella typhimurium-infected mice

immune system phenotype

abnormal macrophage physiology
- macrophages (adherent peritoneal exudates cells, PECs) stimulated with LPS show a reduced induction of ROIs than wild-type macrophages at all LPS concentrations

abnormal neutrophil physiology
- mutant polymorphonuclear leukocytes (PMNs) show poorer induction of reactive oxygen intermediates (ROIs) upon LPS stimulation compared to wild-type; NO production is significantly less in mutant PMNs

decreased acute inflammation
- peak footpad swelling in response to carrageenan injection is reduced compared to wild-type mice

decreased follicular B cell number
- decrease in IgD^hi IgM^lo mature follicular B cells

decreased neutrophil cell number
- total leukocyte numbers are not significantly altered compared to wild-type, but significantly reduced peripheral PMN frequency in blood is observed in mutants

decreased susceptibility to experimental autoimmune encephalomyelitis
- mice show slower induction of experimental autoimmune encephalomyelitis (EAE) and milder clinical disease than wild-type mice

impaired myelopoiesis
- frequency of monocytic/granulocytic precursors (myeloid CFUs) is significantly reduced compared to wild-type bone marrow
- number of monocytic and granulocytic-lineage cells is significantly reduced in mutant bone marrow

impaired neutrophil phagocytosis
- phagocytic ability of PMNs is somewhat lower, but not significantly, compared to wild-type

increased susceptibility to bacterial infection induced morbidity/mortality
- in Salmonella typhimurium-infected mice

increased susceptibility to induced colitis
- dextran sulfate sodium-induced colitis results in significant weight loss in wild-type mice by day 10 of DSS treatment while mutants do not exhibit any weight loss at that time

Genotype: Btk^xid/Y
CBA/HN-Btk

cellular phenotype

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells

hematopoietic system phenotype

decreased B cell number
- spleens have only ~22% immunoglobulin-bearing cells compared to ~50% in controls

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells

decreased splenocyte number
- number of nucleated spleen cells (~60 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

immune system phenotype

decreased B cell number
- spleens have only ~22% immunoglobulin-bearing cells compared to ~50% in controls

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells

decreased splenocyte number
- number of nucleated spleen cells (~60 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

Genotype: Btk^xid/Btk^xid
CBA/HN-Btk

cellular phenotype

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells
- Background Sensitivity - proliferative response in B cells from females is drastically lower than in cells from female mutants on CBA/HN * DBA/2N background

immune system phenotype

abnormal lymphopoiesis
- incidence of small lymphocytes is slightly lower, but absolute population is not, compared to controls

abnormal pre-B cell morphology
- incidence of pre-B cells is slightly reduced, but absolute population is comparable to controls

autoimmune response
- mice do not develop autoantibodies (anti-dsDNA or any IgG antinuclear autoantibodies)

decreased B cell number
- incidence of B lymphocytes is slightly lower, but absolute population is not, compared to controls
- Background Sensitivity - numbers (22%) are less than female mutants on CBA/HN * DBA/2N background (40%)
- spleens have only ~22% immunoglobulin-bearing cells compared to ~50% in controls

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells
- Background Sensitivity - proliferative response in B cells from females is drastically lower than in cells from female mutants on CBA/HN * DBA/2N background

decreased splenocyte number
- Background Sensitivity - females have significantly less than females on the CBA/HN * DBA/2N background which have (~90 x 10⁶/spleen)
- number of nucleated spleen cells (~60 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

hematopoietic system phenotype

abnormal bone marrow cell number
- number of nucleated cells is higher in mutants than in controls

abnormal lymphopoiesis
- incidence of small lymphocytes is slightly lower, but absolute population is not, compared to controls

abnormal pre-B cell morphology
- incidence of pre-B cells is slightly reduced, but absolute population is comparable to controls

decreased B cell number
- incidence of B lymphocytes is slightly lower, but absolute population is not, compared to controls
- Background Sensitivity - numbers (22%) are less than female mutants on CBA/HN * DBA/2N background (40%)
- spleens have only ~22% immunoglobulin-bearing cells compared to ~50% in controls

decreased B cell proliferation
- cultured B cells show little response to B-cell mitogens LPS and poly I:C in comparison to wild-type cells
- Background Sensitivity - proliferative response in B cells from females is drastically lower than in cells from female mutants on CBA/HN * DBA/2N background

decreased splenocyte number
- Background Sensitivity - females have significantly less than females on the CBA/HN * DBA/2N background which have (~90 x 10⁶/spleen)
- number of nucleated spleen cells (~60 x 10⁶/spleen) is significantly lower than in controls (~120 x 10⁶/spleen)

Phenotype Information

Festing Inbred Strain Characteristics: CBA

References

Cancro MP; Sah AP; Levy SL; Allman DM; Schmidt MR; Woodland RT. 2001. xid mice reveal the interplay of homeostasis and Bruton's tyrosine kinase-mediated selection at multiple stages of B cell development. Int Immunol 13(12):1501-14PubMed: 11717191 MGI: J:109858
Amsbaugh DF; Hansen CT; Prescott B; Stashak PW; Barthold DR; Baker PJ. 1972. Genetic control of the antibody response to type 3 pneumococcal polysaccharide in mice. I. Evidence that an X-linked gene plays a decisive role in determining responsiveness. J Exp Med 136(4):931-49PubMed: 4403476 MGI: J:109969
Berning AK; Eicher EM; Paul WE; Scher I. 1980. Mapping of the X-linked immune deficiency mutation (xid) of CBA/N mice. J Immunol 124(4):1875-7PubMed: 7365241 MGI: J:6296

Additional References

Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
Wilson EL; Sherwood EM; King AM; Riley RL. 2003. A phenotypically distinct subset of immature B cells exhibits partial activation, increased survival, and preferential expression of VhS107. Eur J Immunol 33(12):3398-408PubMed: 14635049 MGI: J:90001

Additional - Btk^xid related

Technical Support

Contact Technical Support

Genotyping Protocols
- Pyrosequencing: Btk^xid
- End Point Analysis: Btk^xidEnd Point
- Genotyping resources and troubleshooting
The Jackson Laboratory does not have a PCR genotyping assay for the Btk^xid mutation. The point mutation is a C to T transition at point 219 (Rawlings DJ et al. Science 1993; 261(5119):358-61 [PMID: 8332901]).
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is an exceptional breeder.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Hemizygote
Appearance
- agouti
  Related Genotype: A/A
Citation
When using the CBA/N mouse strain in a publication, please include JAX stock #001011 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MP13 (Maximum)

Pricing & Availability

Available Now

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service	Genotype	Price
	X linked - Homozygous females and hemizygous males for Btk<xid>

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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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.

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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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Licensing Information

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Also Known As: CBA/N

Genetic overview

Research Applications

Base Price

Detailed Description

Control Suggestions

Approximate Controls

Additional Information

Selected References

Btkxid

Allele Symbol: Btkxid

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Genotype

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

Genotype: Btkxid related

Mammalian Phenotype Terms by Genotype

Genotype: Btkxid/Btkxidinvolves: CBA/HN * DBA/2N

cellular phenotype

immune system phenotype

hematopoietic system phenotype

Genotype: Btkxid/Yinvolves: CBA/HN * DBA/2N

cellular phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Btkxid/Btkxidinvolves: C57BL/6 * CBA

mammalian phenotype

Genotype: Btkxid/?involves: BALB/c * CBA/N

cellular phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Btkxid/BtkxidB6.CBA-Btk

hematopoietic system phenotype

immune system phenotype

Genotype: Btkxid/BtkxidCBA/CaHN-Btk/J

digestive/alimentary phenotype

hematopoietic system phenotype

mortality/aging

immune system phenotype

Genotype: Btkxid/YCBA/HN-Btk

cellular phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Btkxid/BtkxidCBA/HN-Btk

cellular phenotype

immune system phenotype

hematopoietic system phenotype

Phenotype Information

References

Additional References

Additional - Btkxid related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Btk^xid

Allele Symbol: Btk^xid

Genotype: Btk^xid related

Genotype: Btk^xid/Btk^xid
involves: CBA/HN * DBA/2N

Genotype: Btk^xid/Y
involves: CBA/HN * DBA/2N

Genotype: Btk^xid/Btk^xid
involves: C57BL/6 * CBA

Genotype: Btk^xid/?
involves: BALB/c * CBA/N

Genotype: Btk^xid/Btk^xid
B6.CBA-Btk

Genotype: Btk^xid/Btk^xid
CBA/CaHN-Btk/J

Genotype: Btk^xid/Y
CBA/HN-Btk

Genotype: Btk^xid/Btk^xid
CBA/HN-Btk

Additional - Btk^xid related