CD13 is a novel mediator of monocytic/endothelial cell adhesion.

CD13 is a novel mediator of monocytic/endothelial cell adhesion.
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CD13是单核细胞/内皮细胞粘附的新型介体。

DOI:
10.1189/jlb.1107802
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发表时间:
2008-08
影响因子:
5.5
通讯作者:
Shapiro LH
Shapiro LH
中科院分区:
医学3区
文献类型:
--
作者:
Mina-Osorio P;Winnicka B;O'Conor C;Grant CL;Vogel LK;Rodriguez-Pinto D;Holmes KV;Ortega E;Shapiro LH

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在炎症过程中,细胞表面粘附分子引导循环白细胞粘附和迁移穿过内衬血管的内皮细胞以到达损伤部位。跨膜分子CD 13在单核细胞和内皮细胞上表达,并已被证明介导同型细胞粘附,这可能意味着CD 13在炎性单核细胞运输中的作用。在这里,我们表明,单克隆抗体或病毒配体的CD 13的连接和聚集以信号转导依赖的方式有效地诱导骨髓细胞/内皮细胞粘附,涉及单核细胞骨架重排和丝状伪足形成。用可溶性重组(r)CD 13治疗可阻断这种CD 13依赖性粘附,来自单核细胞和内皮细胞的CD 13分子存在于同一免疫复合物中,表明CD 13直接参与粘附相互作用。活化的单核细胞粘附于固定的重组CD 13的事实加强了这一概念。此外,在腹膜炎小鼠模型中使用抗CD 13抗体治疗导致腹膜白细胞浸润减少,表明CD 13在体内白细胞运输中的潜在作用。因此,这项工作支持了CD 13生物学的新方向,这些细胞表面分子作为真正的分子界面,诱导和参与关键的炎症细胞相互作用。
During inflammation, cell surface adhesion molecules guide the adhesion and migration of circulating leukocytes across the endothelial cells lining the blood vessels to access the site of injury. The transmembrane molecule CD13 is expressed on monocytes and endothelial cells and has been shown to mediate homotypic cell adhesion, which may imply a role for CD13 in inflammatory monocyte trafficking. Here, we show that ligation and clustering of CD13 by mAb or viral ligands potently induce myeloid cell/endothelial adhesion in a signal transduction‐dependent manner involving monocytic cytoskeletal rearrangement and filopodia formation. Treatment with soluble recombinant (r)CD13 blocks this CD13‐dependent adhesion, and CD13 molecules from monocytic and endothelial cells are present in the same immunocomplex, suggesting a direct participation of CD13 in the adhesive interaction. This concept is strengthened by the fact that activated monocytic cells adhere to immobilized recombinant CD13. Furthermore, treatment with anti‐CD13 antibodies in a murine model of peritonitis results in a decrease in leukocyte infiltration into the peritoneum, suggesting a potential role for CD13 in leukocyte trafficking in vivo. Therefore, this work supports a new direction for CD13 biology, where these cell surface molecules act as true molecular interfaces that induce and participate in critical inflammatory cell interactions.
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