Wernersson S, Kleinau S, Heyman B
Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden.
Scand J Immunol. 2000 Dec;52(6):563-9. doi: 10.1046/j.1365-3083.2000.00813.x.
Immunoglobulin (Ig)G and IgE antibodies enhance the humoral response in vivo to soluble antigens with which they form complexes. In vitro, antigen is targeted to B cells by IgE antibodies and to macrophages and dendritic cells (DCs) by IgG, thus leading to increased antigen presentation to specific T cells. Possibly these mechanisms are also responsible for antibody-mediated enhancement in vivo. We now address the question of whether IgG- and/or IgE-antigen complexes can prime for delayed-type hypersensitivity (DTH), a reaction known to require primed T helper (Th)1 cells. Mice were immunized with IgG-anti-2,4,6-trinitrophenyl (TNP)/BSA-TNP or IgE-anti-TNP/BSA-TNP. Mice given BSA-TNP alone or BSA-TNP in complete Freund's adjuvans (CFA) were used as controls. DTH and IgG-anti-BSA levels were measured after subsequent challenge with BSA. A potent BSA-specific antibody response was induced by IgE- or IgG-complexed antigen as well as by CFA/antigen but DTH-reactions were only observed in mice immunized with CFA/antigen. Both IgE and IgG enhanced the production of BSA-specific IgG1, IgG2a and IgG2b, although the most pronounced enhancement was seen in the production of IgG1. These findings suggest that Th2 cells rather than Th1 cells are involved in the immune response to IgG- and IgE-immune complexes.
免疫球蛋白(Ig)G和IgE抗体可增强体内对与之形成复合物的可溶性抗原的体液免疫反应。在体外,IgE抗体将抗原靶向B细胞,IgG则将抗原靶向巨噬细胞和树突状细胞(DC),从而导致向特定T细胞的抗原呈递增加。这些机制可能也负责体内抗体介导的增强作用。我们现在探讨IgG和/或IgE-抗原复合物是否能引发迟发型超敏反应(DTH)的问题,已知该反应需要经致敏的辅助性T(Th)1细胞。用IgG-抗2,4,6-三硝基苯(TNP)/牛血清白蛋白(BSA)-TNP或IgE-抗-TNP/BSA-TNP免疫小鼠。单独给予BSA-TNP或在完全弗氏佐剂(CFA)中给予BSA-TNP的小鼠用作对照。在用BSA进行后续攻击后,测量DTH和IgG-抗-BSA水平。IgE或IgG复合抗原以及CFA/抗原均可诱导强烈的BSA特异性抗体反应,但仅在用CFA/抗原免疫的小鼠中观察到DTH反应。IgE和IgG均增强了BSA特异性IgG1、IgG2a和IgG2b的产生,尽管在IgG1的产生中观察到最明显的增强。这些发现表明,Th2细胞而非Th1细胞参与了对IgG和IgE免疫复合物的免疫反应。