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Carries a deletion of the endogenous murine J segments of the Ig heavy chain locus
In homozygotes, all four JH gene segments are absent, resulting in cells that cannot produce a complete, recombined version of the variable region of the heavy chain
Have no detectable IgM or IgG in the sera
A low level (about 1% of normal) of rearrangement of the light chain kappa gene family is detected in total bone marrow
Cells of the B lineage are drastically altered both in developmental progression and in cell quantity
Contain no mature (immunoglobulin-bearing) B-lymphocytes in the spleen, bone marrow, lymph nodes, peripheral blood or peritoneum
T-lymphocyte development appears to proceed normally, based on surface phenotype and quantity of cells in the spleen; splenic lymphocytes are enriched for T cells due to the B cell deficit
Provides a null background useful for gene replacement experimentation in normal immune response and autoimmune diseases
Useful for studying non-B cell activity in pathogen-induced disease and mechanisms of antibody gene assembly and expression
- For use in syngeneic experiments, the Jh mouse is 96% congenic to the BALB/c background and may successfully engraft some cell lines of BALB/c origin
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Genetic Background: BALB/c Background
The Jh mouse was developed by Dennis Huszar et al. at GenPharm International. The model was created by targeting the Jh gene in AB01 embryonic stem cells derived from 129/SvEv mice and injecting the targeted cells into C57BL/6J blastocysts. Heterozygotes on a C57BL/6J background were intercrossed to generate homozygous targeted mutation mice. Yale University received stock from GenPharm in 1992. The mice were then backcrossed several generations to a C.B-Igh-1 b congenic background. The mice were then backcrossed two generations (N2) to a BALB/c inbred background and intercrossed to homozygosity. The colony is maintained through homozygous matings.
Wild type for Nnt mutation
Chen J, Trounstine M, Alt FW, Young F, Kurahara C, Loring JF, Huszar D. (1993) Immunoglobulin Gene Rearrangement in B Cell Deficient Mice Generated by Targeted Deletion of the JH Locus. Int Immunol,5(6): 647-656.