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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >EphB2-mediated interactions are essential for proper migration of T cell progenitors during fetal thymus colonization.
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EphB2-mediated interactions are essential for proper migration of T cell progenitors during fetal thymus colonization.

机译：EphB2介导的相互作用对于胎儿胸腺定植期间T细胞祖细胞的正确迁移至关重要。

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摘要

The ephrin-Eph ligand receptor pair is known to control the repulsion/adhesion process in different tissues, including the immune system. Herein, we evaluated the role of EphB2 receptors in T cell progenitor migration during in vitro thymus colonization and to ECM or chemokine stimuli. EphB2 and their ligands, ephrin-B1 and ephrin-B2, are expressed in BM-derived progenitors, and EphB2(-/-) cells had diminished thymus colonization capacity. Conversely, EphB2(LacZ) cells, which maintain a preserved ephrin-binding domain, were capable of colonizing WT thymuses similarly to WT progenitors, highlighting the importance of reverse signals transmitted to normal fetal thymus. However, the EphB2 receptor expressed by microenvironmental cells also drives progenitor immigration, as recolonization of EphB2-deficient fetal thymuses was compromised profoundly. Additionally, we observed lower depositions of ECM and chemokines on EphB2-deficient thymuses but no changes in their receptor expression on BM-derived progenitors and developing thymocytes. Migration of EphB2-deficient progenitors and thymocytes was also reduced through ECM or chemokine stimuli. Furthermore, ephrin-B1 costimulation also inhibited haptotaxis and chemotaxis of WT but not EphB2(LacZ) cells, demonstrating the specific involvement of EphB2 signaling on T cell progenitor migration. Our data suggest the relevance of a nonactivated EphB2 for regulating T cell progenitor migration and its modulation upon ephrin-B engagement.
机译：已知ephrin-Eph配体受体对可控制包括免疫系统在内的不同组织中的排斥/粘附过程。在本文中，我们评估了EphB2受体在体外胸腺定植期间向T细胞祖细胞迁移以及对ECM或趋化因子刺激的作用。 EphB2及其配体，ephrin-B1和ephrin-B2，在BM来源的祖细胞中表达，并且EphB2（-/-）细胞的胸腺定殖能力降低。相反，EphB2（LacZ）细胞保持着保留的ephrin结合结构域，能够像野生型祖细胞一样定殖野生型胸腺，突显了传递至正常胎儿胸腺的反向信号的重要性。但是，微环境细胞表达的EphB2受体也驱使祖细胞迁移，因为EphB2缺陷型胎儿胸腺的再定植已受到严重损害。此外，我们观察到EphB2缺陷型胸腺上ECM和趋化因子的沉积降低，​​但是在BM来源的祖细胞和发育中的胸腺细胞上它们的受体表达没有变化。缺乏EphB2的祖细胞和胸腺细胞的迁移也通过ECM或趋化因子刺激而减少。此外，ephrin-B1共刺激也抑制WT的触觉趋化和趋化性，但不抑制EphB2（LacZ）细胞，这表明EphB2信号传导对T细胞祖细胞迁移的特定参与。我们的数据表明，未激活的EphB2与调节T细胞祖细胞迁移及其对ephrin-B结合的调控具有相关性。

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