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

了解血管渗漏综合征(VLS)的发病机制 白介素2，我们研究了光镜和电子显微镜的变化 小鼠肺、肝、脾、肾和心脏的早期 用白介素2连续注射4d后形成VLS模型。 这些研究揭示了对内皮细胞的相当大的损害 在肺和肝脏的小静脉和小静脉中。此外，还有 淋巴样细胞穿过内皮的频繁部位，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”的方式堆积在血管周围 空格。我们的研究表明，体内的直接相互作用 活化的淋巴细胞和内皮细胞导致细胞毒作用 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.