Transendothelial migration of human basophils
Transendothelial migration of human basophils
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DOI：
10.4049/jimmunol.173.8.5189
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发表时间：
2004-10-15
影响因子：
4.4
通讯作者：
Hirai, K
中科院分区：
文献类型：
--
作者：
Iikura, M;Ebisawa, M;Hirai, K
在过敏反应期间，嗜碱性粒细胞从血液区室迁移到炎症部位，在那里它们与嗜酸性粒细胞协同发挥效应细胞的作用。由于跨内皮迁移 (TEM) 是细胞外渗的重要步骤，因此我们首次使用 HUVEC 研究嗜碱性粒细胞 TEM。用 IL-1beta 处理 HUVEC 显着增强嗜碱性粒细胞 TEM，而 CCR3 特异性配体 eotaxin/CCL11 的存在进一步增强了这种效果。除了 CCR3 配体之外，MCP-1/CCL2 在嗜碱性粒细胞 TEM 上也具有活性。尽管基质细胞衍生因子-1/CXCL12（一种 CXCR4 配体）未能在新鲜分离的嗜碱性粒细胞中诱导 TEM，但在 24 小时培养的细胞中引起了强烈的 TEM。 IL-3 通过增加趋化反应来增强嗜碱性粒细胞 TEM。用抗-CD18 mAb 处理细胞可抑制穿过激活的 HUVEC 的自发 TEM，但用抗-CD29 mAb 则不会，并且用抗-ICAM-1 mAb 处理 HUVEC 也能抑制这种情况。单独的抗 VCAM-1 mAb 不能抑制 TEM，但与抗 ICAM-1 mAb 联合使用时显示出叠加的抑制作用。相反，抗 CD29 mAb 和抗 CD18 mAb 显着抑制嗜酸细胞趋化因子和 IL-3 介导的 TEM。这些结果表明β（2）整合素在嗜碱性粒细胞TEM中起主要作用，但β（1）整合素也参与其中，特别是在细胞因子/趋化因子刺激的嗜碱性粒细胞的TEM中。总之，嗜碱性粒细胞 TEM 的调节特征与报道的嗜酸性粒细胞的调节特征非常相似。因此，我们的结果支持了先前关于嗜碱性粒细胞和嗜酸性粒细胞之间密切关系的论点，并表明这两种细胞类型的体内动力学相似。
During allergic reactions, basophils migrate from the blood compartment to inflammatory sites, where they act as effector cells in concert with eosinophils. Because transendothelial migration (TEM) represents an essential step for extravasation of cells, for the first time we have studied basophil TEM using HUVEC. Treatment of HUVEC with IL-1beta significantly enhanced basophil TEM, which was further potentiated by the presence of a CCR3-specific ligand, eotaxin/CCL11. In addition to CCR3 ligands, MCP-1/CCL2 was also active on basophil TEM. Although stromal cell-derived factor-1/CXCL12, a CXCR4 ligand, failed to induce TEM in freshly isolated basophils, it caused strong TEM in 24-h cultured cells. IL-3 enhanced, basophil TEM by increasing the chemokinetic response. Spontaneous TEM across activated HUVEC was inhibited by treatment of cells with anti-CD18 mAb, but not with anti-CD29 mAb, and also by treatment of HUVEC with anti-ICAM-1 mAb. Anti-VCAM-1 mAb alone failed to inhibit TEM, but showed an additive inhibitory effect in combination with anti-ICAM-1 mAb. In contrast, eotaxin- and IL-3-mediated TEM was significantly inhibited by anti-CD29 mAb as well as anti-CD18 mAb. These results indicate that beta(2) integrins play the primary role in basophil TEM, but beta(1) integrins are also involved, especially in TEM of cytokine/chemokine-stimulated basophils. In conclusion, the regulatory profile of basophil TEM is very similar to that reported for eosinophils. Our results thus support the previous argument for a close relationship between basophils and eosinophils and suggest that the in vivo kinetics of these two cell types are similar.