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首页> 外文期刊>Current Immunology Reviews >BOB.1/OBF.1 - A Critical Regulator of B Cell Function
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BOB.1/OBF.1 - A Critical Regulator of B Cell Function

机译：BOB.1 / OBF.1-B细胞功能的关键调节剂

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The transcriptional coactivator BOB.1/OBF.1 binds as a ternary complex with the transcription factors Oct-1 and Oct-2 to DNA and induces octamer-dependent transcription. BOB.1/OBF.1 was shown to be necessary at multiple stages of B cell development, in the bone marrow as well as at late stages in secondary lymphoid organs. Bone marrow B cells from BOB.1/OBF.1-deficient mice show increased apoptosis accompanied with decreased expression levels of the anti-apoptotic protein Bcl2. Although transgenic B cell-specific expression of Bcl2 rescued the numbers and maturation of BOB.1/OBF.1-deficient B cells in the bone marrow as well as in peripheral lymphoid organs, the B cell function was still severely impaired. The most prominent characteristic of BOB.1/OBF.1 knock-out mice is the complete failure to form germinal centers upon immunization with thymic-dependent antigens and consequently a massive defect in production of secondary Ig isotypes. In addition, the marginal zone B cell compartment, first line defence against blood born antigens, is virtually absent in BOB.1/OBF.1 -/- animals. A large number of genes specifically expressed in B cells contain octamer motifs in their regulatory regions, but only a small number of BOB.1/OBF.1 dependent genes are described yet. To understand the molecular basis of BOB.1/OBF.1 function in B cell development we and others searched for BOB.1/OBF.1 target genes. A large number of BOB.1/OBF.1-dependent genes were identified, which are involved in different aspects of lymphocyte development and signaling, supporting the critical regulatory role of BOB.1/OBF.1 for lymphocyte function. Here we summarize recent developments highlighting the central role that BOB.1/OBF.1 plays in B lymphocytes.
机译：转录共激活因子BOB.1 / OBF.1与转录因子Oct-1和Oct-2作为三元复合物结合到DNA上，并诱导八聚体依赖性转录。已证明，在骨髓以及继发性淋巴器官的晚期B细胞发育的多个阶段，BOB.1 / OBF.1都是必需的。来自BOB.1 / OBF.1缺陷小鼠的骨髓B细胞显示出凋亡增加，同时抗凋亡蛋白Bcl2的表达水平降低。尽管Bcl2的转基因B细胞特异性表达挽救了骨髓以及周围淋巴器官中BOB.1 / OBF.1缺陷B细胞的数量和成熟，但B细胞功能仍然受到严重损害。 BOB.1 / OBF.1敲除小鼠的最显着特征是完全免疫后无法用胸腺依赖性抗原免疫形成生发中心，因此在继发Ig同种型的生产中存在巨大缺陷。另外，在BOB.1 / OBF.1-/-动物中实际上不存在针对血液中携带的抗原的一线防御的边缘区B细胞区室。在B细胞中特异性表达的大量基因在其调控区均含有八聚体基序，但仅描述了少数BOB.1 / OBF.1依赖性基因。为了了解BOB.1 / OBF.1在B细胞发育中起作用的分子基础，我们和其他人一起寻找了BOB.1 / OBF.1靶基因。大量BOB.1 / OBF.1依赖基因被确定，它们参与淋巴细胞发育和信号转导的不同方面，支持BOB.1 / OBF.1对淋巴细胞功能的关键调节作用。在这里，我们总结了最近的发展，突出了BOB.1 / OBF.1在B淋巴细胞中发挥的核心作用。

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