CD22 deficient mutant mice exhibit a reduction in recirculating mature B cells in the bone marrow and fewer transitional B cells in the spleen. Splenic and peripheral B cells express lower levels of membrane bound IgM than wildtype. B cell activation is abnormal in mutant mice, with enhanced Ca2+ mobilization after stimulation. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, B cell development and T cell independent immune response.
Lars Nitschke, University of Erlangen
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No expression of the targeted gene's protein product is detected on the cell surface, as determined by flow cytometry analysis of splenocytes from homozygotes. Mutants exhibit a reduction in recirculating mature B cells in the bone marrow and fewer transitional B cells in the spleen. Splenic and peripheral B cells express lower levels of membrane bound IgM than wildtype. B cell activation is abnormal in mutant mice, with enhanced Ca2+ mobilization after stimulation. Lipopolysaccaharide (LPS) challenge results in an increased proliferative response. CD22 deficient B cells have a shorter than average lifespan when compared to wildtype B cells. T-cell independent immune responses are impaired. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, B cell development and T cell independent immune response.
This strain was transferred from the collection of the Consortium for Functional Glycomics.
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon11, which encodes the transmembrane domain. The construct was electroporated into C57BL/6 derived BL/6-III embryonic stem (ES) cells.
Correctly targeted ES cells were injected into recipient blastocysts. The donating investigator reported that the mice were backcrossed to the C57BL/6 (see SNP note below) background for 10 generations before arriving at The Jackson Laboratory.
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.
|Allele Name||targeted mutation 1, Marinus C Lamers|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Cd22, CD22 antigen|
|Strain of Origin||C57BL/6J|
|Molecular Note||Exon 11, encoding the transmembrane domain, was disrupted by the insertion of a neomycin cassette. Flow cytometric analysis showed an absence of surface expression on splenocytes isolated from homozygous mutant mice.|
|Mutations Made By|| |
Peter Sobieszczuk, Consortium for Functional Glycomics,TSRI
When maintaining a live colony, these mice can be bred as homozygotes.
When using the C57BL/6-Cd22tm1Lam /J mouse strain in a publication, please cite the originating article(s) and include JAX stock #006940 in your Materials and Methods section.