Delespesse G, Sarfati M
Allergy Research Laboratory, Notre-Dame Hospital, Montreal, Quebec, Canada.
Ric Clin Lab. 1988 Apr-Sep;18(2-3):75-92. doi: 10.1007/BF02918876.
B cell-derived IgE-BFs (sCD23) are cleavage fragments of surface Fc epsilon R II. Their production is increased by IL4 and suppressed by IFN-gamma and IFN-alpha. IgE-BFs are likely to play a role in the regulation of human IgE synthesis as shown by the following two observations: i. MabER specifically blocks both the spontaneous IgE by synthesis by atopic B cells and the IL4-induced IgE synthesis by normal lymphocytes, ii. purified IgE-BFs enhance the IL4-induced and the spontaneous IgE synthesis. Soluble fragments of Fc epsilon R II also display BCGF-like activity although the exact structure of these fragments is not yet identified. The cDNA coding for Fc epsilon R II has been cloned and functionally expressed. The predicted amino acid sequence reveals no homology between human and rodent IgE-BFs indicating that they are unrelated molecules.
B细胞衍生的IgE结合因子（sCD23）是表面FcεR II的裂解片段。IL-4可增加其产生，而IFN-γ和IFN-α可抑制其产生。如下两个观察结果表明，IgE结合因子可能在人类IgE合成的调节中发挥作用：i. MabER特异性阻断特应性B细胞自发合成IgE以及正常淋巴细胞IL-4诱导的IgE合成；ii. 纯化的IgE结合因子增强IL-4诱导的和自发的IgE合成。FcεR II的可溶性片段也表现出类似BCGF的活性，尽管这些片段的确切结构尚未确定。编码FcεR II的cDNA已被克隆并进行了功能表达。预测的氨基酸序列显示，人类和啮齿动物的IgE结合因子之间没有同源性，表明它们是不相关的分子。
