降低实验性胰腺癌肿瘤内皮中基础和刺激的白细胞粘附。

J Schmidt, E Ryschich, S M Maksan, J Werner, M M Gebhard, C Herfarth, E Klar
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引用次数: 12

摘要

背景:免疫活性细胞与肿瘤内皮之间的相互作用是有效免疫应答的必要条件。在本研究中,我们评估了大鼠实验性胰腺癌肿瘤血管和健康胰腺小静脉中静息和CD11b/ cd18介导的白细胞粘附。方法:将实体瘤碎片(1 mm3)插入活体显微镜下惰性聚甲基丙烯酸甲酯透明平板(n = 12),观察肿瘤微循环、白细胞-肿瘤-内皮相互作用以及化学引诱剂n -甲酰基甲硫氨酸亮基苯丙氨酸(fMLP)和血小板活化因子(PAF)对白细胞粘附的影响。结果:与健康胰腺小静脉相比,肿瘤血管中的白细胞粘附明显降低。fMLP和PAF均可显著增加正常胰腺小静脉的白细胞粘附性。暴露于这些趋化物质后,肿瘤血管中的白细胞粘附没有变化。结论:实验性胰腺癌恶性血管中静息和受刺激的整合素依赖性白细胞粘附明显减少,这可能是其逃避免疫控制的重要机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reduced basal and stimulated leukocyte adherence in tumor endothelium of experimental pancreatic cancer.

Background: The interaction between immunocompetent cells and tumor endothelium is essential for an effective immunological response. In the present study, we evaluated resting and CD11b/CD18-mediated leukocyte adhesion in tumor vessels of experimental pancreatic cancer and in healthy pancreatic venules in the rat.

Methods: Solid tumor fragments (1 mm3) were interposed intrapancreatically between inert transparent polymethylmetacrylate plates for intravital microscopy (n = 12) by which tumor microcirculation, leukocyte-tumor-endothelium interaction, and the effect of the chemoattractants N-formyl-methioninleucylphenylalanine (fMLP) and platelet-activating factor (PAF) on leukocyte adherence was investigated.

Results: Leukocyte adhesion in pancreatic tumor vessels was significantly reduced compared to healthy pancreatic venules. Both fMLP and PAF dramatically increased leukocyte adherence in normal pancreatic venules. No change in leukocyte adhesion was present in tumor vessels after exposure to these chemotactic substances.

Conclusion: Resting and stimulated integrin-dependent leukocyte adhesion is strongly reduced in malignant vessels of experimental pancreatic cancer, which may be an important mechanism to escape immune control.

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