CBA/CaHN-Btkxid/J mice have a mutation in the Bruton's tyrosine kinase gene (Btk), and are a model of human X-linked immunodeficiency. They have a B-lymphocyte-specific defect that results in an inability to launch an antibody response to thymus-independent type II antigens, although they do produce normal amounts of antibody in response to some protein antigens. They have low serum IgM and IgG3 and a reduced number of B-cells. Moreover, the B-cells that are present have a reduced surface IgM to IgD ratio, which suggests a disorder in B-cell maturation.
 
 
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Removal of this mouse colony is imminent. If live mice are needed for your studies, it is advised that they be ordered immediately. After removal, the mice will be available from a cryorecovery. CBA/CaHN-Btkxid/J mice have a mutation in the Bruton's tyrosine kinase gene (Btk), and are a model of human X-linked immunodeficiency. They have a B-lymphocyte-specific defect that results in an inability to launch an antibody response to thymus-independent type II antigens, although they do produce normal amounts of antibody in response to some protein antigens. They have low serum IgM and IgG3 and a reduced number of B-cells. Moreover, the B-cells that are present have a reduced surface IgM to IgD ratio, which suggests a disorder in B-cell maturation.