Cd8alpha-deficient BXSB.Yaa mice (BXSB.Yaa Cd8a-/- or BXSB.Yaa Cd8α-/-) are a BXSB-congenic strain carrying a null mutation of the CD8 antigen alpha chain. The suppressor CD8+ T cell-deficiency of BXSB.Yaa Cd8a-/- mice leads to an accelerated and more severe form of spontaneous lupus-like autoimmune syndrome compared to BXSB/MpJ inbred mice. These BXSB.Yaa Cd8a-/- mice may be useful in studying how MHC class I-dependent CD8+ T cells normally attenuate spontaneous lupus-like autoimmune syndrome.
Dr. Derry Roopenian, The Jackson Laboratory
|Allele Type||Gene Symbol||Gene Name|
|Targeted||Cd8a||CD8 antigen, alpha chain|
|Allele Type||Gene Symbol||Gene Name|
|Spontaneous||Yaa||accelerated autoimmunity and lymphoproliferation transposition|
Cd8alpha-deficient BXSB.Yaa mice (BXSB.Yaa Cd8a-/- or BXSB.Yaa Cd8α-/-) are a BXSB/MpJ-congenic strain carrying a null mutation of the CD8 antigen alpha chain.
BXSB/MpJ inbred males (Stock No. 000740) develop a spontaneous lupus-like autoimmune syndrome: mortality starts at ~13 weeks of age with 50% lethality by ~30 weeks and 76% lethality by ~40 weeks. BXSB/MpJ inbred females develop a greatly attenuated form of autoimmune disease.
Homozygous (Cd8a-/-) mice are viable and fertile. Homozygotes are deficient in functional cytotoxic T-cells, but exhibit normal helper T-cell development and function. Compared to BXSB/MpJ, the suppressor CD8+ T cell-deficiency of BXSB.Yaa Cd8a-/- mice leads to an accelerated and more severe spontaneous autoimmune phenotype. Specifically, mortality in BXSB.Yaa Cd8a-/- males starts at ~12-15 weeks of age with 50% lethality by ~20 weeks of age. Compared to homozygous males, the homozygous females develop a greatly attenuated form of autoimmune disease.
Heterozygous males (BXSB.Yaa Cd8a+/-) develop the BXSB/MpJ autoimmune phenotype. Heterozygous females develop a greatly attenuated form of autoimmune disease because they lack Yaa.
C57BL/6J-congenic mice harboring the Cd8α null allele are described and available from The Jackson Laboratory Repository as Stock No. 002665.
The Cd8α null allele (Cd8atm1Mak) was designed by Dr. Tak Mak (University of Toronto) with a neomycin resistance cassette replacing exon 1 of the Cd8a gene (CD8 antigen alpha chain) on chromosome 6. C57BL/6J-congenic mice harboring this Cd8α null allele are described and available from The Jackson Laboratory Repository as Stock No. 002665.
Dr. Derry C. Roopenian (The Jackson Laboratory) obtained some of these mutant mice and backcrossed them with BXSB/MpJ inbred mice (Stock No. 000740) for 18 generations, and then maintained the colony by breeding homozygous mice together. In 2003, Dr. Roopenian froze embryos from BXSB.Yaa Cd8a-/- mice at generation N18. In 2013, this frozen stock was transferred to The Jackson Laboratory Repository (Autoimmune Resource) to establish Stock No. 021456. Male mice have the BXSB/MpJ-derived Y chromosome that contains the Y-linked autoimmune accelerator locus (Yaa).
|Allele Name||targeted mutation 1, Tak Mak|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||CD8 KO; CD8-; CD8-KO; CD8KO; CD8alpha-; CD8alpha-; Cd8atm1Mak; Lyt-2-|
|Gene Symbol and Name||Cd8a, CD8 antigen, alpha chain|
|Gene Synonym(s)||BB154331; CD8; Leu2; Ly-2; Ly-2; Ly-35; Ly-35; Ly-B; Lyt-2; Lyt-2; MAL; T-lymphocyte antigen 2; expressed sequence BB154331; lymphocyte antigen 2; lymphocyte antigen 35; p32|
|Strain of Origin||129S2/SvPas|
|Mutations Made By|| |
Dr. Tak Mak, University Health Network/Un of Toronto
|Allele Name||accelerated autoimmunity and lymphoproliferation|
|Allele Synonym(s)||Is(XOfd1-Mid1;Y)1Mp; Tp(X;Y)1Ekw|
|Gene Symbol and Name||Yaa, accelerated autoimmunity and lymphoproliferation transposition|
|Strain of Origin||SB/Le|
To maintain the live colony, homozygous mice may be bred together. Homozygous mice are viable and fertile, but exhibit an accelerated spontaneous autoimmune phenotype compared to BXSB/MpJ inbred mice (Stock No. 000740). Specifically, mortality in BXSB.Yaa Cd8a-/- males starts at ~12-15 weeks of age with 50% lethality by ~20 weeks of age. Compared to males, the BXSB.Yaa Cd8a-/- females develop a greatly attenuated form of autoimmune disease. Heterozygotes will develop the sex-specific autoimmune phenotype of BXSB/MpJ. The expected coat color is white-bellied agouti.
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