动物造模,免疫调节因子缺陷小鼠模型 z-bio 2023-10-09 1064

　　1. Gene knockout mice with B cell defects. In B cell deficient Igh-6 gene knockout mice, homozygotes lack mature B cells and cannot express membrane bound IgM. This mouse is mainly used to study the function of B cells in the immune system. For example, after immunization with the attenuated strain of rabbit fever, it can produce a considerable number of CD4+T cells and CD8+T cells, and can use IFN and nitrogen oxides to control its infection. However, mice cannot survive after the second infection with the attenuated strain of rabbit fever. But if the initial B cells are replaced with B cells before the second infection, they can survive after the second infection of the rabbit disease virus. This elucidates the role of B cells in resisting rabbit fever.

　　2. Chemokine (C-C motif) receptor 2 gene knockout mice with chemokine and chemokine receptor deficiency, homozygous mice can survive and reproduce, with normal phenotype and behavior, but with type 1 immune response deficiency in mice. IFN- α A decrease in quantity. Ccr2 deficient mice with BALB/C background have functional defects in vesicle monocytes, and blood monocytes cannot aggregate neutrophils.

　　three γ Interferon deficient mice γ- Interferon gamma (IFN) gene knockout mice, homozygous mice can survive and reproduce, and exhibit normal phenotypes in the absence of pathogenic agents. However, when the pathogenic agent is present, the macrophages of deficient mice produce relatively less antibacterial products and type II MHC antigens. Infection of B6.129S7-IFN tmlTs/J mice with slow spreading lymphocytic choroidal meningitis virus strain (LCMV) can lead to chronic disease, while in the control group, the infection can be quickly cleared.

　　4. Interleukin-4 (IL-4) gene knockout mice showed normal development of homozygous T cells and B cells, but levels of IgG1 and IgE significantly decreased. They completely lack the cell-dependent classical IgG1 dominant immune response, and mice infected with nematodes can only produce undetectable IgE.

　　After infection with Borrelia burgdorferi, BALB/c background IL-4 knockout mice produced significantly high titers of spirochete specific IgG2a and IgG1.

　　5. Interleukin-6 (IL-6) gene knockout mice exhibit normal homozygous development, but cannot effectively control infection with cowpox virus or Listeria monocytogenes. A facultative intracellular bacterium can damage the T cell dependent antibody response to vesicular stomatitis virus in mice. Yersinia enterocolitica has stronger toxicity to B6.129S2-Il6 tmlKopf/J mice and is more rapidly cloned in the tissue system.

　　6. Interleukin-12 gene knockout mouse interleukin-12 (interleukin 12a),