Daeron M, Ishizaka K
J Immunol. 1986 Mar 1;136(5):1612-9.
Normal mouse peritoneal macrophages express Fc gamma 2aR, Fc gamma 1/2bR, and Fc epsilon R, whereas B lymphocytes in mesenteric lymph nodes (MLN) bear Fc gamma 2bR, Fc gamma 1R, and Fc epsilon R. Rosette formation of Fc epsilon R+ macrophages and lymphocytes with IgE-coated ox erythrocytes was inhibited by rodent IgE but not by any other isotype of mouse immunoglobulins. In contrast, IgG1 rosettes and IgG2b rosettes of both macrophages and lymphocytes were inhibited not only by homologous isotype but also by IgE, suggesting that IgE has some affinity for Fc gamma 1/2bR on macrophages and for both Fc gamma 1R and Fc gamma 2bR on lymphocytes. Incubation of normal mouse macrophages with mouse IgE for 24 hr resulted in a twofold increase in the proportion of Fc epsilon R+ cells. Mouse IgE can induce Fc epsilon R on B cells as well. Incubation of MLN cells with mouse IgE for 2 to 4 hr, followed by culture of the cells in the absence of IgE, resulted in a 1.8- to 2.9-fold increase in Fc epsilon R+ cells. Determination of Fc gamma R+ cells in the same MLN cells revealed that induction of Fc epsilon R by IgE was accompanied by a substantial decrease in the expression of Fc gamma 1R and Fc gamma 2bR. Induction of Fc epsilon R by IgE on macrophages and lymphocytes requires protein synthesis. In MLN cells, cycloheximide inhibited not only the IgE-induced increase in Fc epsilon R+ cells but also the decrease in Fc gamma 1R+ cells and Fc gamma 2bR+ cells. It was also found that induction of Fc epsilon R by IgE on macrophages was completely inhibited if IgG1 or IgG2b was added to the cells together with IgE. In contrast, IgG2a did not affect the IgE-induced expression of Fc epsilon R on macrophages. In MLN cells, IgG2b but not IgG1 inhibited both IgE-induced increase in Fc epsilon R and decrease in Fc gamma 1R and Fc gamma 2bR. The results indicate that expression of various Fc receptors on lymphocytes is mutually regulated.
正常小鼠腹膜巨噬细胞表达Fcγ2aR、Fcγ1/2bR和FcεR，而肠系膜淋巴结（MLN）中的B淋巴细胞则带有Fcγ2bR、Fcγ1R和FcεR。FcεR+巨噬细胞和淋巴细胞与IgE包被的牛红细胞形成的玫瑰花结形成被啮齿动物IgE抑制，但不被小鼠免疫球蛋白的任何其他同种型抑制。相反，巨噬细胞和淋巴细胞的IgG1玫瑰花结和IgG2b玫瑰花结不仅被同源同种型抑制，也被IgE抑制，这表明IgE对巨噬细胞上的Fcγ1/2bR以及淋巴细胞上的Fcγ1R和Fcγ2bR都有一定亲和力。用小鼠IgE孵育正常小鼠巨噬细胞24小时，导致FcεR+细胞比例增加两倍。小鼠IgE也能诱导B细胞上的FcεR。用小鼠IgE孵育MLN细胞2至4小时，然后在无IgE的情况下培养细胞，导致FcεR+细胞增加1.8至2.9倍。对同一MLN细胞中FcγR+细胞的测定表明，IgE诱导FcεR的同时，Fcγ1R和Fcγ2bR的表达大幅下降。IgE在巨噬细胞和淋巴细胞上诱导FcεR需要蛋白质合成。在MLN细胞中，放线菌酮不仅抑制IgE诱导的FcεR+细胞增加，还抑制Fcγ1R+细胞和Fcγ2bR+细胞的减少。还发现，如果将IgG1或IgG2b与IgE一起加入细胞中，IgE在巨噬细胞上诱导FcεR的作用会被完全抑制。相反，IgG2a不影响IgE诱导的巨噬细胞上FcεR的表达。在MLN细胞中，IgG2b而非IgG1抑制IgE诱导的FcεR增加以及Fcγ1R和Fcγ2bR的减少。结果表明淋巴细胞上各种Fc受体的表达相互调节。
