动物造模,B淋巴细胞缺陷,动物模型 z-bio 2021-10-13 538

　　The B lymphocyte deficiency model is usually clinically manifested as immunoglobulin deficiency and normal cell-mediated immunity. Here, we take the CBA/N mouse as an example. CBA/N mice are characterized by poor function of B lymphocytes and X chain recessive mutants, and their genetic marker is xid. Homozygous female mice (xid/xid) and heterozygous male mice (xid/y) have type II antigens (thymus-independent antigens such as dextran, pneumococcal lipopolysaccharide and double-stranded DNA).

　　"Lack of antibody response to thymus-dependent antigens, low serum IgG and IgM. Transplanting normal mouse bone marrow into xid host can restore B-cell deficiency. In contrast, the bone marrow of xid mice was transplanted into a normal host of the same strain that was irradiated, but still exhibited an abnormal phenotype and no defect in T cell function. This model is the ideal tool to study the development, function and heterogeneity of B lymphocytes, and its pathology is similar to human Bruton gamma globulin deficiency and Wiscot-Aidsh syndrome.