Araake M, Uchiyama T, Imanishi K, Yan X J
Department of Microbiology, Tokyo Women's Medical College, Japan.
Int Arch Allergy Appl Immunol. 1991;96(1):55-61. doi: 10.1159/000235535.
Human umbilical vascular endothelial cells (HUVEC) stimulated with recombinant human IFN-gamma were investigated for expression of HLA class II molecules, toxic shock syndrome toxin-1 (TSST-1)-binding activity and accessory cell (AC) activity in TSST-1-induced T cell activation. HUVEC stimulated with recombinant human IFN-gamma ranging from 10 to 1,000 units/ml for 72 h express HLA class II molecules. Intensity of the expression was dependent on the concentration of IFN-gamma. HUVEC stimulated with 1,000 units/ml of IFN-gamma for 72 h exhibited 125I-TSST-1-binding that was blocked by the unlabeled toxin and monoclonal antibodies (mAb) to DR/DP. The activity was not removed by paraformaldehyde fixation. The IFN-gamma-stimulated HUVEC exhibited AC activity in TSST-1-induced IL-2 production by T cells from human peripheral blood mononuclear cells. The activity was blocked by mAb to DR. The above two activities were also observed in L cells transfected with DR2 genes but not in the unstimulated HUVEC and control L cells. In view of the fact that TSST-1 binds directly to HLA class II molecules and activates human T cells in association with HLA class II molecules on AC, it is likely that the acquisition of TSST-1-binding activity and AC activity in the toxin-induced T cell activation is mediated by the expression of HLA class II molecules. Vascular endothelial cells may play an important role in the development of pathological changes in TSS patients.
研究了用重组人γ干扰素刺激的人脐静脉血管内皮细胞(HUVEC)在中毒性休克综合征毒素-1(TSST-1)诱导的T细胞活化中HLA II类分子的表达、TSST-1结合活性和辅助细胞(AC)活性。用10至1000单位/毫升的重组人γ干扰素刺激HUVEC 72小时,其表达HLA II类分子。表达强度取决于γ干扰素的浓度。用1000单位/毫升的γ干扰素刺激HUVEC 72小时,表现出125I-TSST-1结合,该结合被未标记的毒素和抗DR/DP单克隆抗体(mAb)阻断。该活性不会因多聚甲醛固定而消除。γ干扰素刺激的HUVEC在TSST-1诱导的人外周血单个核细胞T细胞产生白细胞介素-2中表现出AC活性。该活性被抗DR的mAb阻断。在用DR2基因转染的L细胞中也观察到上述两种活性,但在未刺激的HUVEC和对照L细胞中未观察到。鉴于TSST-1直接结合HLA II类分子并与AC上的HLA II类分子结合激活人T细胞,毒素诱导的T细胞活化中TSST-1结合活性和AC活性的获得可能是由HLA II类分子的表达介导的。血管内皮细胞可能在中毒性休克综合征患者病理变化的发展中起重要作用。