LYMPHOCYTES & ENDOTHELIUM IN THE VASCULAR LEAK SYNDROME INDUCED BY INTERLEUKIN-2

目的：了解血管渗漏综合征（VLS）的发生机制， 白细胞介素-2，我们检查了光镜和电镜改变， 肺，肝，脾，肾和心脏的小鼠，其中早期阶段 VLS通过施用白细胞介素-2超过4天而产生。 这些研究揭示了相当大的损害内皮细胞， 在肺和肝的小静脉和小静脉中。 此外还有 淋巴样细胞穿过内皮的常见部位，可能 淋巴因子激活的杀伤细胞，穿透细胞质 通过“暂时性迁移孔”并积聚在血管周围 空间. 我们的研究表明， 活化的淋巴细胞和内皮细胞导致细胞毒性， 内皮细胞

To understand the mechanism of the vascular leak syndrome (VLS) caused by interleukin-2, we examined light and electron microscopic alterations in lung, liver, spleen, kidney and heart of mice in which an early stage of the VLS was produced by the administration of interleukin-2 over 4 days. These studies disclosed considerable damage to endothelial cells especially in venules and small veins of lung and liver. In addition, there were frequent sites of transendothelial passage of lymphoid cells, probably lymphokine-activated killer cells, which penetrated through their cytoplasm by means of "temporary migration pores" and accumulated in the perivascular spaces. Our studies indicate that a direct in vivo interaction between activated lymphocytes and endothelium results in cytotoxicity to endothelial cells.