Heyman B, Tianmin L, Gustavsson S
Department of Pathology, Uppsala University, Sweden.
Eur J Immunol. 1993 Jul;23(7):1739-42. doi: 10.1002/eji.1830230754.
The ability of antigen-specific IgE antibodies to modulate the in vivo antibody response was studied by comparing the antibody response in mice immunized with 2,4,6-trinitrophenyl (TNP)-specific monoclonal IgE followed by bovine serum albumin (BSA)-TNP or with BSA-TNP alone. The serum IgG antibody response against BSA, measured in enzyme-linked immunosorbent assay ELISA, was enhanced up to 100-fold in groups receiving IgE. The enhancement required specific interaction between IgE and antigen, since no effect was seen when unconjugated BSA was used as antigen. Polyclonal activation by IgE/antigen complexes did not occur. IgE given 24 h after specific antigen had no stimulatory capacity. Pretreatment of the mice with Fc epsilon receptor type II (Fc epsilon RII)-specific monoclonal antibody completely inhibited the IgE-mediated enhancement. Thus, the data demonstrate for the first time an in vivo role for Fc epsilon RII in enhancement of specific antibody production.
通过比较用2,4,6-三硝基苯基(TNP)特异性单克隆IgE免疫后再用牛血清白蛋白(BSA)-TNP免疫的小鼠和仅用BSA-TNP免疫的小鼠体内的抗体反应,研究了抗原特异性IgE抗体调节体内抗体反应的能力。在酶联免疫吸附测定(ELISA)中测量的针对BSA的血清IgG抗体反应,在接受IgE的组中增强了高达100倍。这种增强需要IgE与抗原之间的特异性相互作用,因为当使用未结合的BSA作为抗原时未观察到效果。IgE/抗原复合物未发生多克隆激活。在特异性抗原后24小时给予IgE没有刺激能力。用II型Fcε受体(FcεRII)特异性单克隆抗体预处理小鼠完全抑制了IgE介导的增强作用。因此,这些数据首次证明了FcεRII在体内增强特异性抗体产生中的作用。