Hase N, Takai T, Hikida M, Ohmori H
Department of Biotechnology, Faculty of Engineering, Okayama University, Japan.
Int J Immunopharmacol. 1994 Oct;16(10):787-94. doi: 10.1016/0192-0561(94)90052-3.
It was found that an antigen-specific IgE response both in vitro and in vivo was strongly suppressed in the presence of IgG1 monoclonal antibody (mAb) against the antigen. Anti-trinitrophenyl (TNP) IgE response was elicited by the co-culture of C3H B-cells and a conalbumin (CA)-specific helper T-cell clone, D10.G4.1, in the presence of 0.1 microgram/ml TNP-CA. Addition of anti-TNP IgG1 monoclonal antibody (mAb) at 1 microgram/ml to the culture resulted in a marked (> 90%) suppression of anti-TNP IgE formation, while anti-TNP IgG1 and IgM responses were affected to a lesser extent (50-60% suppression). Similar observations were made in in vivo experiments. When 100-200 micrograms of anti-TNP IgG1 mAb was injected i.p. into BDF1 mice prior to immunization with TNP-CA, the anti-hapten (TNP) IgE response as well as the IgE response to the carrier (CA) was suppressed by 80-90%, while anti-TNP IgM production was inhibited by less than 50%. Injection of anti-TNP IgM or IgA mAb showed only marginal effects on anti-TNP IgE production. Spleen cells from anti-TNP IgG1 mAb-treated mice cultured in vitro secreted much lower levels of anti-TNP IgE spontaneously than those from untreated mice. In in vitro and in vivo experiments using the F(ab')2 of anti-TNP IgG1 mAb, an IgG1 mAb with an irrelevant specificity and mAb directed to Fc gamma RII, it was shown that the binding of the IgG1 mAb with the antigen and the interaction of its Fc portion with Fc gamma RII are required for the suppressive effects to be exerted.
研究发现，在存在针对该抗原的IgG1单克隆抗体（mAb）的情况下，体外和体内的抗原特异性IgE反应均受到强烈抑制。抗三硝基苯（TNP）IgE反应是通过在含有0.1微克/毫升TNP-伴清蛋白（CA）的条件下，将C3H B细胞与CA特异性辅助性T细胞克隆D10.G4.1共培养而引发的。向培养物中添加1微克/毫升的抗TNP IgG1单克隆抗体（mAb），导致抗TNP IgE形成受到显著抑制（>90%），而抗TNP IgG1和IgM反应受到的影响较小（抑制50-60%）。在体内实验中也有类似的观察结果。在用TNP-CA免疫之前，将100-200微克的抗TNP IgG1 mAb腹腔注射到BDF1小鼠体内，抗半抗原（TNP）IgE反应以及对载体（CA）的IgE反应被抑制80-90%，而抗TNP IgM产生的抑制率小于50%。注射抗TNP IgM或IgA mAb对抗TNP IgE产生仅显示出轻微影响。与未处理小鼠的脾细胞相比，在体外培养的经抗TNP IgG1 mAb处理小鼠的脾细胞自发分泌的抗TNP IgE水平要低得多。在使用抗TNP IgG1 mAb的F(ab')2、具有不相关特异性的IgG1 mAb以及针对FcγRII的mAb进行的体外和体内实验中，结果表明，IgG1 mAb与抗原的结合及其Fc部分与FcγRII的相互作用是发挥抑制作用所必需的。
