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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A forward genetic screen reveals roles for Nfkbid, Zeb1, and Ruvbl2 in humoral immunity
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A forward genetic screen reveals roles for Nfkbid, Zeb1, and Ruvbl2 in humoral immunity

机译：前瞻性遗传筛选揭示了Nfkbid，Zeb1和Ruvbl2在体液免疫中的作用

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摘要

Using chemical germ-line mutagenesis, we screened mice for defects in the humoral immune response to a type II T-independent immunogen and an experimental alphavirus vector. A total of 26 mutations that impair humoral immunity were recovered, and 19 of these mutations have been positionally cloned. Among the phenovariants were bumble, cellophane, and Worker ascribed to mutations in Nfkbid, Zeb1, and Ruvbl2, respectively. We show that IkBNS, the nuclear lxB-like protein encoded by Nfkbid, is required for the development of marginal zone and peritoneal B-1 B cells and additionally required for extrafollicular antibody responses to T-independent and -dependent immunogens. Zeb1 is also required for marginal zone and peritoneal B-1 B-cell development as well as T-cell development, germinal center formation, and memory B-cell responses. Finally, Ruvbl2 is required for T-cell development and maximal T-dependent antibody responses. Collectively, the mutations that we identified give us insight into the points at which disruption of an antibody response can occur. All of the mutations identified to date directly affect lymphocyte development or function; none have an exclusive effect on cells of the innate immune system.
机译：使用化学种系诱变，我们筛选了小鼠对II型非T型免疫原的体液免疫应答和实验性甲病毒载体的缺陷。总共回收了26个损害体液免疫力的突变，其中19个突变已被位置克隆。在表型变量中，大黄，玻璃纸和Worker分别归因于Nfkbid，Zeb1和Ruvbl2中的突变。我们显示，IkBNS，由Nfkbid编码的核lxB样蛋白，对于边缘区和腹膜B-1 B细胞的发育是必需的，并且对于对T依赖性和依赖性免疫原的卵泡外抗体应答也是必需的。 Zeb1也是边缘区和腹膜B-1 B细胞发育以及T细胞发育，生发中心形成和记忆B细胞反应所必需的。最后，Ruvbl2是T细胞发育和最大的T依赖抗体应答所必需的。总的来说，我们鉴定出的突变使我们深入了解了可能发生抗体反应中断的点。迄今确定的所有突变都直接影响淋巴细胞的发育或功能。没有一种对先天免疫系统的细胞具有排他性作用。

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    Carrie N. Arnold; Elaine Pirie; Pia Dosenovic; Gerald M. Mdnerney; Yu Xia; Nathaniel Wang; Xiaohong Li; Owen M. Siggs; Gunilla B. Karlsson Hedestam; Bruce Beutler;

  • 作者单位

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden;

    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden;

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

    Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden;

    Department of Genetics, The Scripps Research Institute, La Jolla, CA 92037;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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