Excessive vulnerability of herpes-infected endothelium to lymphokine-activated lymphocytes: a possible role in lethal viral pneumonitis following bone marrow transplantation.
Excessive vulnerability of herpes-infected endothelium to lymphokine-activated lymphocytes: a possible role in lethal viral pneumonitis following bone marrow transplantation.
复制标题
疱疹感染的内皮对淋巴因子激活的淋巴细胞过度脆弱：骨髓移植后致死性病毒性肺炎的可能作用。
DOI：
--
复制
发表时间：
1988
期刊：
影响因子：
--
通讯作者：
H. Jacob
中科院分区：
文献类型：
--
作者：
G. Vercellotti;D. Kotasek;H. Jacob
1.淋巴因子激活的杀伤细胞在体外对人脐静脉内皮细胞具有细胞毒作用。2.LAK细胞的细胞毒作用与丝氨酸酯酶活性有关。3.骨髓移植患者产生的LAK细胞对培养内皮细胞的杀伤作用明显高于正常人，这与其丝氨酸酯酶含量和NK细胞表型比例升高有关。4.单纯疱疹病毒感染血管内皮细胞4小时后，内皮细胞更易受LAK细胞介导的损伤。5.因此，骨髓移植患者体内有“预置”的淋巴细胞，极有可能成为淋巴因子激活的杀伤细胞。这些细胞具有NK表型，容易产生细胞毒性丝氨酸酯酶活性，并表现出损伤血管内皮细胞的倾向，尤其是病毒感染的内皮细胞。我们认为，这种倾向可能是感染疱疹病毒的骨髓移植患者遭受严重内皮炎和致死性肺出血的原因。
1. Lymphokine-activated killer cells are cytotoxic to human umbilical vein endothelial cells in vitro. 2. Cytotoxic efficiency of LAK cells correlates with serine esterase activity. 3. LAK cells generated from bone marrow transplant patients, as compared to normal volunteers, are significantly more cytotoxic for cultured endothelium, which correlates with their elevated serine esterase content and phenotypic NK-cell proportion. 4. Endothelium infected with herpes simplex virus for very brief periods (4 hr) becomes even more vulnerable to LAK cell-mediated injury. 5. Thus, bone marrow transplant patients harbor "primed" lymphocytes, highly liable to become lymphokine-activated killer cells. These cells have an NK phenotype, readily generate cytotoxic serine esterase activity, and manifest a proclivity to damage vascular endothelium--especially virally infected endothelium. We suggest this proclivity may underlie the severe endotheliitis and lethal pulmonary hemorrhage suffered by bone marrow transplant patients infected with herpesviruses.