Spontaneous mutation in the Cd79b gene leads to a block in B-lymphocyte development at the C' (early pre-B) stage.
We discovered B-lymphocyte-deficient mice within a group of B10.A-CD45.1 mice, and established that this deficiency was a recessively inherited trait. Gene mapping and sequence analysis showed a mutation in the third exon of the Cd79b gene (c.224G>A) that leads to the generation of a stop codon (W75X) in the mutant mouse. Fluorescent-activated cell sorting analysis of bone marrow cells showed that the mutant mice did not express the CD79B antigen. To establish where the block in development happens, we analyzed CD43(pos)B220(pos) B-lymphocyte precursors present in the mutant mice and found that the fraction C' (corresponding to early pre-B lymphocytes) was absent in the mutant mouse, whereas fractions B and C showed a relative accumulation. As expected, we found no IgG or IgA in mutant mice. These results suggest that this CD79b-mutant strain may be a useful tool for immunological research in human immunodeficiencies.
Shulzhenko
N
N
Ghost lab, T Cell Memory and Tolerance Section, Laboratory of Cellular and Molecular Immunology (LCMI), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Bethesda, MD 20892, USA. shulzhenkon@niaid.nih.gov
Morgun
A
A
Matzinger
P
P
D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology* / Q000276:immunology*; D001483:Base Sequence; D051925:CD79 Antigens / Q000235:genetics* / Q000276:immunology*; D002454:Cell Differentiation; D007070:Immunoglobulin A / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D051379:Mice; D009154:Mutation
D051925:CD79 Antigens; C497884:Cd79b protein, mouse; D007070:Immunoglobulin A; D007074:Immunoglobulin G