Ijichi S, Yamano Y, Osame M, Hall W W
Third Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Sakuragaoka, Japan.
Cell Immunol. 1996 Nov 1;173(2):312-6. doi: 10.1006/cimm.1996.0283.
The kinetics of thymidine incorporation into fractionated T lymphocytes responding to bacterial superantigens were compared to those of cells activated by phytohemagglutinin (PHA). Evident differences between the kinetics of cell proliferation induced by PHA-P and staphylococcal enterotoxin B (SEB) emerged after Day 4 of culture. PHA-P-induced proliferative responses of peripheral blood mononuclear cells (PBMCs) and fractionated cells were apparent on Day 4 because of the presence of accessory cells in the initial cell suspensions. This gradually diminished in correlation with the decline of accessory cells in the cultures. The SEB-induced cell growth (PBMCs and CD4+ cells), however, continued until Day 9 of the culture. This finding suggests the reciprocal usage of MHC class II molecules to present SEB by activated T lymphocytes for superantigen-induced T cell activation and suggests that superantigen-related immune activation may depend in part on the potential of activated T lymphocytes to mediate reciprocal cell-to-cell interactions in the presence of superantigens. The decline observed in the CD8+ cell response to SEB and toxic shock syndrome toxin-1 after Day 4 was revived by exogenous recombinant interleukin-2 (rIL-2) supplementation, suggesting that the consequent autocrine or paracrine secretion of IL-2 from the responding cells is essential for subsequent cell proliferation. SEB-induced cell proliferation was significantly suppressed by anti-CD11a (lymphocyte function-associated antigen-1; LFA-1, alpha-chain) monoclonal antibody, and the inhibitory effect was most obvious in 6-day cultured CD8+ lymphocytes. The results suggest that the lymphocyte response associated with the cell-to-cell copresentation of superantigens involves LFA-1 molecules as an accessory factor, particularly in CD8+ lymphocytes.
将胸苷掺入对细菌超抗原作出反应的分次T淋巴细胞的动力学,与由植物血凝素(PHA)激活的细胞的动力学进行了比较。在培养第4天后,PHA-P和葡萄球菌肠毒素B(SEB)诱导的细胞增殖动力学之间出现了明显差异。由于初始细胞悬液中存在辅助细胞,PHA-P诱导的外周血单核细胞(PBMC)和分次细胞的增殖反应在第4天很明显。这与培养物中辅助细胞的减少相关而逐渐减弱。然而,SEB诱导的细胞生长(PBMC和CD4+细胞)持续到培养第9天。这一发现表明,活化的T淋巴细胞相互利用MHC II类分子来呈递SEB以进行超抗原诱导的T细胞活化,并表明超抗原相关的免疫激活可能部分取决于活化的T淋巴细胞在存在超抗原的情况下介导细胞间相互作用的潜力。在第4天后观察到的CD8+细胞对SEB和中毒性休克综合征毒素-1的反应下降,通过外源性重组白细胞介素-2(rIL-2)补充得以恢复,这表明反应细胞随后自分泌或旁分泌IL-2对于后续细胞增殖至关重要。抗CD11a(淋巴细胞功能相关抗原-1;LFA-1,α链)单克隆抗体显著抑制了SEB诱导的细胞增殖,并且抑制作用在培养6天的CD8+淋巴细胞中最为明显。结果表明,与超抗原的细胞间共同呈递相关的淋巴细胞反应涉及LFA-1分子作为辅助因子,特别是在CD8+淋巴细胞中。