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无丙种球蛋白血症(aly)突变小鼠的体细胞超突变和类别转换缺陷。

Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice.

作者信息

Shinkura R, Matsuda F, Sakiyama T, Tsubata T, Hiai H, Paumen M, Miyawaki S, Honjo T

机构信息

Department of Medical Chemistry, Center for Molecular Biology and Genetics, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606, Japan.

出版信息

Int Immunol. 1996 Jul;8(7):1067-75. doi: 10.1093/intimm/8.7.1067.

DOI:10.1093/intimm/8.7.1067
PMID:8757952
Abstract

The alymphoplasia (aly) mutation of mice causes the systemic absence of lymph nodes, Peyer's patches and well-defined lymphoid follicles in the spleen. We found that antibody responses are elicited, albeit weakly, to either T cell-dependent or T cell-independent antigen by aly/aly mutants. However, isotype switching was defective. The T cell-dependent immune response was not elicited in splenectomized aly/aly mice. Neither hypermutation nor germinal center formation was observed in aly/aly mice. These results suggest that T-B collaboration requires either lymph nodes or spleen, and that hypermutation and affinity maturation depend on germinal center formation.

摘要

小鼠的无淋巴细胞生成(aly)突变导致全身淋巴结、派伊尔结以及脾脏中界限分明的淋巴滤泡缺失。我们发现,aly/aly突变体对T细胞依赖性或T细胞非依赖性抗原均可引发抗体反应,尽管反应较弱。然而,其同种型转换存在缺陷。在脾切除的aly/aly小鼠中未引发T细胞依赖性免疫反应。在aly/aly小鼠中既未观察到超突变,也未观察到生发中心形成。这些结果表明,T细胞与B细胞的协作需要淋巴结或脾脏,并且超突变和亲和力成熟依赖于生发中心的形成。

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