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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Three chemokine receptors cooperatively regulate homing of hematopoietic progenitors to the embryonic mouse thymus
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Three chemokine receptors cooperatively regulate homing of hematopoietic progenitors to the embryonic mouse thymus

机译：三种趋化因子受体协同调节造血祖细胞向胚胎小鼠胸腺的归巢

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摘要

The thymus lacks self-renewing hematopoietic cells, and thymopoi-esis fails rapidly when the migration of progenitor cells to* the thymus ceases. Hence, the process of thymus homing is an essential step for T-cell development and cellular immunity. Despite decades of research, the molecular details of thymus homing have not been elucidated fully. Here, we show that chemotaxis is the key mechanism regulating thymus homing in the mouse embryo. We determined the number of early thymic progenitors in the thymic rudiments of mice deficient for one, two, or three of the chemokine receptor genes, chemokine (C-C motif) receptor 9 (CaS), chemokine (C-C motif) receptor 7 (Ccr7), and chemokine (C-X-C motif) receptor 4 (CxcrA). In the absence of all three chemokine receptors, thymus homing was reduced about 100-fold both before and after vascu-larization of the thymic rudiment. In the absence of only two of these three chemokine receptor genes, thymus homing was much less affected (only two- to 10-fold), indicating that the chemotactic regulation of thymus homing is remarkably robust. Our results reveal the redundant roles of Ccr9, Ccr7, and Cxcr4 for thymic homing and provide a framework to examine the regulation of progenitor homing in the postnatal thymus.
机译：胸腺缺乏自我更新的造血细胞，并且当祖细胞向胸腺的迁移停止时，胸腺快速消失。因此，胸腺归巢的过程是T细胞发育和细胞免疫的重要步骤。尽管进行了数十年的研究，但尚未完全阐明胸腺归巢的分子细节。在这里，我们显示趋化性是调节小鼠胚胎中胸腺归巢的关键机制。我们确定了缺乏一个，两个或三个趋化因子受体基因，趋化因子（CC基序）受体9（CaS），趋化因子（CC基序）受体7（Ccr7）的小鼠的胸腺残基中的早期胸腺祖细胞的数量，和趋化因子（CXC基序）受体4（CxcrA）。在没有所有三种趋化因子受体的情况下，在胸腺残基血管化之前和之后，胸腺归巢减少了约100倍。在这三个趋化因子受体基因中只有两个不存在的情况下，对胸腺归巢的影响要小得多（只有2到10倍），这表明对胸腺归巢的趋化调节非常强大。我们的研究结果揭示了Ccr9，Ccr7和Cxcr4在胸腺归巢中的冗余作用，并提供了一个框架来检查产后胸腺中祖细胞归巢的调节。

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    Lesly Calderón; Thomas Boehm;

  • 作者单位

    Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, D-79108 Freiburg, Germany;

    Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, D-79108 Freiburg, Germany;

  • 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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  • 正文语种 eng
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