Stimulation of endothelial cell binding of lymphocytes by tumor necrosis factor.
Stimulation of endothelial cell binding of lymphocytes by tumor necrosis factor.
复制标题
肿瘤坏死因子刺激内皮细胞与淋巴细胞的结合。
DOI：
10.4049/jimmunol.139.6.1855
复制
发表时间：
1987
影响因子：
4.4
通讯作者：
M. Ziff
中科院分区：
文献类型：
--
作者：
D. Cavender;Y. Saegusa;M. Ziff
淋巴因子和单核细胞因子已被报道影响内皮细胞的形态和功能。在这里描述的实验中，我们已经证明了重组肿瘤坏死因子(TNF)刺激T淋巴细胞与人脐静脉内皮细胞融合单层的黏附。肿瘤坏死因子诱导的粘附性增加是EC特异性的，因为与肿瘤坏死因子预先孵育淋巴细胞不会改变结合，人皮肤成纤维细胞与肿瘤坏死因子预先孵育不会增加其对淋巴细胞的低粘附性。低至0.01U/m l(1pg/m l)的肿瘤坏死因子可刺激T-EC结合。在动力学实验中，EC与肿瘤坏死因子预孵育4小时可获得最佳的粘附性。经多聚甲醛固定后，经肿瘤坏死因子处理的内皮细胞保持了较高的粘附性，提示肿瘤坏死因子通过增加淋巴细胞表面受体的表达或可获得性来刺激其结合。尽管针对T细胞上淋巴细胞功能相关抗原1α或β链的抗体显著抑制未刺激的T-EC结合，但这种抗体对肿瘤坏死因子诱导的EC粘附性的增加没有影响，表明这种结合的增加是由于EC膜上产生了另一种结合受体。这些发现提供了进一步的证据，证明细胞因子通过刺激内皮细胞对循环淋巴细胞的黏附而参与慢性炎症反应中单核细胞的动员。
Lymphokines and monokines have been reported to affect endothelial cell (EC) morphology and function. In experiments here described, we have demonstrated that recombinant tumor necrosis factor (TNF) stimulates the adhesion of T lymphocytes to confluent monolayers of human umbilical vein EC. The increase in adhesion induced by TNF was EC-specific inasmuch as preincubation of the lymphocytes with TNF did not alter binding, and preincubation of human dermal fibroblasts with TNF did not increase their inherently low adhesiveness for lymphocytes. Stimulation of T-EC binding occurred after treatment of the EC with as little as 0.01 U/ml (1 pg/ml) of TNF. In kinetic experiments, preincubation of EC with TNF for 4 hr resulted in optimal adhesion. TNF-treated EC retained their increased adhesiveness after fixation with paraformaldehyde, suggesting that TNF stimulated binding by increasing the expression or accessibility of EC surface receptors for lymphocytes. Although antibodies to the lymphocyte function-associated antigen 1 alpha- or beta-chains on the T cell markedly inhibited unstimulated T-EC binding, such antibodies had no effect on the increase in EC adhesiveness induced by TNF, indicating that the increased binding resulted from the generation of an alternate binding receptor on the EC membrane. These findings provide additional evidence that cytokines participate in the mobilization of mononuclear cells in the chronic inflammatory reaction by stimulation of the adhesiveness of endothelium for circulating lymphocytes.