Rothermel A L, Gilbert K M, Weigle W O
Research Institute of Scripps Clinic, Department of Immunology, La Jolla, California 92037.
Cell Immunol. 1991 Jun;135(1):1-15. doi: 10.1016/0008-8749(91)90249-b.
Human gamma globulin-specific T helper cell (Th) clones, activated by HGG in the presence of antigen (Ag)-presenting cells, stimulated polyclonal B cell proliferation. Both Th1 and Th2 clones induced B cell proliferation, but Th1 clones were generally 5- to 10-fold less efficient than Th2 in this capacity. Th1 and Th2 each induced proliferation of both small and large B cells, although Th1 induced less B cell proliferation than Th2, regardless of B cell size. Th1-induced B cell proliferation was increased significantly by stimulating the Th1 clones with immobilized anti-CD3 mAb. The B cell response to Ag-activated Th1 clones was also increased by the addition of rIL-4 or culture supernatants from activated Th2 clones, and this enhancement was abolished by addition of anti-IL-4 mAb. The differential capacity of the Th subsets to stimulate B cells could not be attributed to differences in the degree of Ag-induced activation of the Th clones as reflected by Th proliferation or Th expression of activation markers, RL388 Ag, IL-2R, or TfR. Taken together the results suggest that even though Th1 and Th2 are similarly activated by Ag-presenting cells, Ag-activated Th2 interact more effectively with B cells than Ag-activated Th1. It is possible that inefficient interaction and subsequent intercellular signaling between Th1 and B cells results in inefficient Th1-induced B cell proliferation, and that this deficiency may be circumvented by signals (e.g., lymphokines) provided by Th2, or by the stimulation of Th1 with plate-bound anti-CD3 Ab rather than Ag.
在抗原呈递细胞存在的情况下，由人丙种球蛋白（HGG）激活的人γ球蛋白特异性辅助性T细胞（Th）克隆可刺激多克隆B细胞增殖。Th1和Th2克隆均能诱导B细胞增殖，但在此能力方面，Th1克隆的效率通常比Th2低5至10倍。Th1和Th2均可诱导小B细胞和大B细胞增殖，尽管无论B细胞大小，Th1诱导的B细胞增殖均少于Th2。通过用固定化抗CD3单克隆抗体刺激Th1克隆，可显著增加Th1诱导的B细胞增殖。添加重组白细胞介素-4（rIL-4）或活化的Th2克隆的培养上清液也可增强B细胞对Ag激活的Th1克隆的反应，而添加抗IL-4单克隆抗体可消除这种增强作用。Th亚群刺激B细胞的能力差异不能归因于Ag诱导的Th克隆激活程度的差异，如通过Th增殖或Th活化标志物、RL388 Ag、IL-2R或TfR的表达所反映的那样。综合这些结果表明，尽管Th1和Th2被抗原呈递细胞以类似方式激活，但Ag激活的Th2与B细胞的相互作用比Ag激活的Th1更有效。Th1与B细胞之间低效的相互作用及随后的细胞间信号传导可能导致Th1诱导的B细胞增殖效率低下，并且这种缺陷可能通过Th2提供的信号（如淋巴因子）或通过用板结合抗CD单克隆抗体而非Ag刺激Th1来克服。
