Verma D S, Spitzer G, Beran M
Am J Hematol. 1982 Jun;12(4):403-10. doi: 10.1002/ajh.2830120412.
To investigate the mechanisms that modulate granulocyte-macrophage colony-stimulating activity (GM-CSA) and burst promoting activity (BPA) elaboration, we studied human peripheral blood-derived monocyte-macrophage (M0) and T-lymphocyte (TL) interaction. Coincubation of live M0 with autologous TL at a 1:3 ratio in the presence of 1% phytohemagglutinin synergistically increased GM-CSA (6 of 6 experiments) and BPA (4 of 6 experiments) (P less than 0.002). Prior treatment of M0 with cycloheximide or actinomycin D significantly (P less than 0.002) diminished this M0's capacity to collaborate with TL. Mitomycin C treatment did not. Live M0 also enhanced TL-derived GM-CSA (P less than 0.002) and BPA (P less than 0.001). This enhancement was again compromised by prior cycloheximide or actinomycin D treatment, but not by mitomycin C treatment. Further experiments in which we blocked DR antigen on M0 membrane with monoclonal anti-DR antibodies suggested that M0 required their membrane DR antigen to collaborate with TL in elaborating GM-CSA and BPA.
为了研究调节粒细胞-巨噬细胞集落刺激活性(GM-CSA)和爆式促进活性(BPA)产生的机制,我们研究了人外周血来源的单核细胞-巨噬细胞(M0)与T淋巴细胞(TL)的相互作用。在存在1%植物血凝素的情况下,将活的M0与自体TL以1:3的比例共同孵育,可协同增加GM-CSA(6个实验中有6个)和BPA(6个实验中有4个)(P小于0.002)。用环己酰亚胺或放线菌素D预先处理M0可显著(P小于0.002)降低其与TL协同作用的能力。丝裂霉素C处理则无此作用。活的M0还增强了TL来源的GM-CSA(P小于0.002)和BPA(P小于0.001)。这种增强作用再次因预先用环己酰亚胺或放线菌素D处理而受损,但不受丝裂霉素C处理的影响。我们用单克隆抗DR抗体阻断M0膜上的DR抗原的进一步实验表明,M0在产生GM-CSA和BPA时需要其膜DR抗原与TL协同作用。