Arrenbrecht S, Mitchell G F
Immunology. 1975 Mar;28(3):485-95.
When immune spleen cells of mice immunized to a hapten carrier preparation 4 days previously were transferred to normal syngeneic hosts, they began to produce 7S antibody (presumably of the IgG class), provided that relatively small numbers of cells (about 1/10 spleen equivalent) were transferred. Increasing the number of transferred cells resulted in less IgG antibody formed. Depletion of the immune spleen cells of T cells by treatment with anti-theta serum and complement prevented IgG antibody formation. IgG antibody production by untreated and anti-therta serum-treated immune spleen cells could be enhanced (reinduced) by addition of small numbers of cells enriched for carrier-activated T cells. These suggest that T cells are necessary to stimulate antigen-activated B cells into IgG antibody production. Larger numbers of 'carrier-activated T cells' depressed IgG antibody production. Both enhancement and depression could be demonstrated to be antigen-specific. IgG antibody production high numbers of transferred immune spleen cells could be induced by treating the cells prior to transfer with suboptimal amounts of anti-theta serum and complement. It is argued that this results from the elimination of a T cell-dependent suppressor influence arising during a normal immune response.
当4天前用半抗原载体制剂免疫的小鼠免疫脾细胞被转移到同基因正常宿主时,只要转移相对少量的细胞(约1/10脾当量),它们就开始产生7S抗体(可能是IgG类)。增加转移细胞的数量会导致形成的IgG抗体减少。用抗θ血清和补体处理使免疫脾细胞中的T细胞耗竭可阻止IgG抗体的形成。通过添加少量富含载体激活T细胞的细胞,未处理的和抗θ血清处理的免疫脾细胞的IgG抗体产生可得到增强(再诱导)。这些表明T细胞对于刺激抗原激活的B细胞产生IgG抗体是必需的。大量“载体激活的T细胞”会抑制IgG抗体的产生。增强和抑制均可证明是抗原特异性的。用次优量的抗θ血清和补体在转移前处理细胞,可诱导大量转移免疫脾细胞产生IgG抗体。有人认为,这是由于消除了正常免疫反应过程中产生的T细胞依赖性抑制作用所致。