Isobe K, Nakashima I
Department of Immunology, Nagoya University School of Medicine, Japan.
Infect Immun. 1992 Nov;60(11):4832-7. doi: 10.1128/iai.60.11.4832-4837.1992.
Staphylococcal enterotoxin A (SEA)- or SEB-stimulated T-lymphocyte proliferation was suppressed by the addition of high numbers of murine peritoneal macrophages or rat peritoneal or alveolar macrophages, whereas lower numbers of murine peritoneal macrophages enhanced the T-lymphocyte response. Suppression was associated with the increase of accumulation of nitrite, a product of nitric oxide, in the culture supernatants. This macrophage-mediated suppression was totally reversed by the addition of NG-monomethyl-L-arginine, a homolog of L-arginine, indicating that macrophage-mediated suppression of T-lymphocyte proliferation was mediated through the nitric oxide-synthesizing pathway activity. Macrophages in large numbers spontaneously produced nitric oxide in culture supernatant fluids. By the addition of autologous or allogeneic spleen cells but not thymocytes to SEA- or SEB-stimulated macrophage culture, nitric oxide production was greatly increased. When T lymphocytes in spleen cells were killed by antibody before addition to macrophage culture, nitric oxide production was diminished to the basal level. These results suggest that in addition to the action to support the process of T-lymphocyte activation by SEA or SEB, macrophages display a feedback regulatory action on the SEA- or SEB-stimulated T-cell proliferative response by releasing nitric oxide through interaction between macrophages and activated T lymphocytes.
添加大量小鼠腹腔巨噬细胞、大鼠腹腔巨噬细胞或肺泡巨噬细胞可抑制葡萄球菌肠毒素A（SEA）或SEB刺激的T淋巴细胞增殖，而少量小鼠腹腔巨噬细胞则增强T淋巴细胞反应。抑制作用与培养上清液中亚硝酸盐（一氧化氮的产物）积累的增加有关。添加L-精氨酸的同系物NG-单甲基-L-精氨酸可完全逆转这种巨噬细胞介导的抑制作用，表明巨噬细胞介导的T淋巴细胞增殖抑制作用是通过一氧化氮合成途径的活性介导的。大量巨噬细胞在培养上清液中自发产生一氧化氮。向SEA或SEB刺激的巨噬细胞培养物中添加自体或同种异体脾细胞而非胸腺细胞，可使一氧化氮产量大幅增加。在将脾细胞中的T淋巴细胞添加到巨噬细胞培养物之前，用抗体将其杀死，一氧化氮产量会降至基础水平。这些结果表明，巨噬细胞除了具有支持SEA或SEB激活T淋巴细胞过程的作用外，还通过巨噬细胞与活化的T淋巴细胞之间的相互作用释放一氧化氮，对SEA或SEB刺激的T细胞增殖反应发挥反馈调节作用。
