Mutant mice

Athymic Nude

Hsd: Athymic Nude-Foxn1^nu
Hsd: Athymic Nude-Foxn1^nu/Foxn1⁺

Albino. Derived from a nucleus colony obtained from the National Cancer Institute, Frederick, Maryland. This immunodeficient model was originally thought to be a Balb/c congenic, but was later reported by NCI to be outbred.

Characteristics

The nu allele on chromosome 11 is an autosomal recessive mutation
Dysfunctional rudimentary thymus
Litter average: 7
Phenotypically hairless (sparse hair growth possible)
T-cell deficient
B-cells function normal
No generation of cytotoxic effector cells
No graft versus host response
Foxn1^nu/Foxn1⁺ heterozygotes do not show partial expression of the nu phenotype

Research use

Oncology
Transplantation
Tumor cell growth
Immunology
Autoimmune disease
Antibody production
Sentinel model heterozygous - Foxn1nu/Foxn1+

Other available data

Hematology
Clinical chemistry
Proven model with extensive references

BALB/c Nude

BALB/cOlaHsd-Foxn1^nu
BALB/cOlaHsd-Foxn1^nu/Foxn1⁺

Albino. Institute of Animal Genetics, Edinburgh to Laboratory Animals Centre, Carshalton, to GD Searle, High Wycombe, to Olac (now Envigo) in 1978.

Characteristics

The nu allele on chromosome 11 is an autosomal recessive mutation
Dysfunctional rudimentary thymus
Phenotypically hairless (sparse hair growth possible)
T-cell deficient
B-cells function normal
No generation of cytotoxic effector cells
No graft versus host response
Foxn1^nu/Foxn1⁺ heterozygotes do not show partial expression of the nu phenotype

Research use

Oncology
Transplantation
Tumor cell growth
Immunology
Autoimmune disease
Antibody production
Sentinel model heterozygous - Foxn1nu/Foxn1+

Other available data

Hematology
Clinical chemistry
Proven model with extensive references

NMRI Nude

HsdCpb:NMRI-Foxn1^nu
HsdCpb:NMRI-Foxn1^nu/Foxn1⁺

Albino. Derived from a nucleus colony obtained from the Laboratory Animals Centre, Carshalton, UK. To TNO-CPB (now Envigo) in 1972.

Characteristics

The nu allele on chromosome 11 is an autosomal recessive mutation
Dysfunctional rudimentary thymus
Phenotypically hairless (sparse hair growth possible)
T-cell deficient
B-cells function normal
No generation of cytotoxic effector cells
No graft versus host response
Foxn1^nu/Foxn1⁺ heterozygotes do not show partial expression of the nu phenotype

Research use

Oncology
Transplantation
Tumor cell growth
Immunology
Autoimmune disease
Antibody production
Sentinel model heterozygous - Foxn1nu/Foxn1+

Other available data

Hematology
Clinical chemistry
Proven model with extensive references

SCID

C.B-17/IcrHan^®Hsd-Prkdc^scid
C.B-17/IcrHsd-Prkdc^scid

Albino. Harlan acquired from the Fox Chase Cancer Center, Philadelphia, Pennsylvania, in 1991. Harlan became Envigo in 2015.

Han^® is a registered trademark of Envigo

Characteristics

Autosomal recessive, single nucleotide polymorphism within Prkdc gene on chromosome 16
Severe combined immunodeficiency affecting T- and B-cell development
Natural Killer (NK) cell, macrophage and granulocyte cell numbers and function are normal
As SCID mice age, a variable percentage become “leaky” from the spontaneous development of functional T- and B-lymphocytes
Highly susceptible to opportunistic viral and bacterial infection

Research use

Oncology
Transplantation
Tumor cell growth
Immunology

SCID/Beige

C.B-17/IcrHsd-Prkdc^scidLyst^bg

Albino. Harlan acquired from the Fox Chase Cancer Center, Philadelphia, Pennsylvania, in 1991. Harlan became Envigo in 2015.

Characteristics

Autosomal recessive, single nucleotide polymorphism within Prkdc gene on chromosome 16
Autosomal recesive, beige (bg-J) mutation on chromosome 13
Severe combined immunodeficiency affecting T- and B- cell development
Severe lymphopenia
Diminished Natural Killer (NK) cell activity relative to other SCID models
Rudimentary thymus
Highly susceptible to opportunistic viral and bacterial infection

Research use

Oncology
Teratology
Transplantation
Tumor cell growth
Immunology

Other available data

Proven model with extensive references

NOD.SCID

NOD.CB17-Prkdc^scid/NCrHsd

Albino. Received by National Cancer Institute, Frederick, Maryland in 2004 from National Institutes of Health, Bethesda, Maryland. Harlan Laboratories acquired from National Cancer Institute in 2006. Harlan became Envigo in 2015.

Characteristics

Autosomal recessive, single nucleotide polymorphism within Prkds gene on chromosome 16
Severe combined immunodeficiency affecting T- and B- cell development
Natural killer (NK) cell, macrophage and granulocyte cell numbers and function are reduced
As SCID models, a variable percentage become leaky from the spontaneous development of functional T- and B-lymphocytes
Highly susceptible to opportunistic viral and bacterial infection
Development of autoimmune diabetes does not occur due to severe combined immunodeficiency
Spontaneous thymic lymphomas

Research use

Oncology
Transplantation
Tumor cell growth
Immunology

Other available data

Hematology
12-week growth,

Other strains of mutant mice:

Diabetic (db/db)
BKS.Cg-+Lepr^db/+Lepr^db/OlaHsd
BKS.Cg-(lean)/OlaHsd

Obese (ob/ob)
B6.V-Lep^ob/Lep^ob/OlaHsd
B6.V-(lean)/OlaHsd

Albino C57BL/6
C57BL/6/BrdCrHsd-Tyr^c

SHrN™ (“Shorn”) Hairless NOD.SCID
NOD.Cg-PrkdcscidHrhr/NCrHsd

MF1 Nude
HsdOla:MF1-Foxn1^nu
HsdOla:MF1-Foxn1^nu/Foxn1⁺

NMRI Nude
HsdCpb:NMRI-Foxn1^nu
HsdCpb:NMRI-Foxn1^nu/Foxn1⁺MRL/MpOlaHsd-Tnfrsf6^LPR
Hsd:NIHS-Lyst^bg-JFoxn1^nuBtk^xid
Hsd:NIHS-Lyst^bg-JFoxn1^nu/Foxn1⁺Btk^xid

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