Romagnani S, Del Prete G, Maggi E, Ricci M
J Immunol. 1987 Mar 15;138(6):1744-9.
Seventy-eight clones established from tonsillar T lymphocytes of two nonallergic children were tested under different experimental conditions for their ability to induce in vitro IgE synthesis by B cells from allergic or nonallergic donors. After 24 hr preactivation with phytohemagglutinin (PHA), 11 out of 32 CD4+ clones from the first and 17 out of 36 CD4+ clones from the second tonsil donor showed the ability to induce IgE synthesis in vitro by B cells from both allergic and nonallergic individuals, whereas none of 10 CD8+ clones nor T blasts of PHA-induced cell lines obtained from unfractionated T cell suspensions of the same tonsils had such an effect. Seven of the 11 T cell clones from the first tonsil donor active on IgE production after pre-activation with PHA also induced IgE synthesis in vitro by nonallergic and allergic B cells upon stimulation with anti-CD3 monoclonal antibody. Under the same experimental conditions, virtually all of the T cell clones able to induce IgE synthesis in vitro by target B cells showed the ability to stimulate IgG and IgM production as well. T cell clones were also established from the peripheral blood of a nonallergic donor and were tested for their ability to induce IgE synthesis in autologous B cells. After preactivation with PHA, seven out of 35 CD4+ clones induced the production of detectable amounts of both IgE and IgG in autologous B cells. The addition to the cultures of PHA-stimulated unfractionated T cells inhibited in a dose-dependent manner the IgE but not the IgG synthesis induced by an autologous helper T cell clone in autologous B cells. Taken together, these data indicate that a remarkable proportion of human T cell clones upon triggering of the CD3 molecular complex were able to provide help for the synthesis of IgE in B cells from both allergic and nonallergic individuals. The successful induction of IgE synthesis by single T cell clones was apparently related to the lack of concomitant suppressor activity to which IgE-producing cells appeared to be exquisitely sensitive.
从两名非过敏儿童的扁桃体T淋巴细胞建立的78个克隆,在不同实验条件下,检测它们诱导来自过敏或非过敏供体的B细胞体外合成IgE的能力。用植物血凝素(PHA)预激活24小时后,来自第一个扁桃体供体的32个CD4 +克隆中的11个以及来自第二个扁桃体供体的36个CD4 +克隆中的17个,显示出能够诱导来自过敏和非过敏个体的B细胞体外合成IgE的能力,而来自相同扁桃体未分离的T细胞悬液的10个CD8 +克隆或PHA诱导的细胞系的T母细胞均无此作用。在第一个扁桃体供体的11个对PHA预激活后对IgE产生有活性的T细胞克隆中,有7个在用抗CD3单克隆抗体刺激后,也能诱导非过敏和过敏B细胞体外合成IgE。在相同实验条件下,几乎所有能够诱导靶B细胞体外合成IgE的T细胞克隆也显示出刺激IgG和IgM产生的能力。还从一名非过敏供体的外周血中建立了T细胞克隆,并检测它们诱导自体B细胞合成IgE的能力。用PHA预激活后,35个CD4 +克隆中的7个诱导自体B细胞产生可检测量的IgE和IgG。将PHA刺激的未分离T细胞加入培养物中,以剂量依赖性方式抑制自体辅助性T细胞克隆在自体B细胞中诱导的IgE合成,但不抑制IgG合成。综上所述,这些数据表明,相当比例的人类T细胞克隆在触发CD3分子复合物后,能够为来自过敏和非过敏个体的B细胞合成IgE提供帮助。单个T细胞克隆成功诱导IgE合成显然与缺乏伴随的抑制活性有关,而产生IgE的细胞似乎对这种抑制活性极为敏感。