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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
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Genetic Background: BALB/c Background
Origin: 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.
Genetics: 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