Defrance T, Aubry J P, Rousset F, Vanbervliet B, Bonnefoy J Y, Arai N, Takebe Y, Yokota T, Lee F, Arai K
J Exp Med. 1987 Jun 1;165(6):1459-67. doi: 10.1084/jem.165.6.1459.
Human rIL-4 is able to induce the expression of low-affinity receptors for IgE (Fc epsilon RL/CD23) on resting B lymphocytes, as determined by the binding of either the anti Fc epsilon RL/CD23-specific mAb 25 or IgE. Stimulation of B cells with insolubilized anti-IgM antibody increases the number of cells expressing Fc epsilon RL/CD23 upon culturing with IL-4 and enhances the level of Fc epsilon RL/CD23 expression on these cells. Fc epsilon RL/CD23 induction is specific for IL-4 since IL-1 alpha, IL-2, IFN-gamma, B cell-derived B cell growth factor (BCGF), and a low-molecular-weight BCGF were ineffective. IFN-gamma strongly inhibited the induction of Fc epsilon RL/CD23 by IL-4.
人重组白细胞介素-4(rIL-4)能够诱导静息B淋巴细胞表达低亲和力IgE受体(FcεRⅡ/CD23),这是通过抗FcεRⅡ/CD23特异性单克隆抗体25或IgE的结合来确定的。用不溶性抗IgM抗体刺激B细胞,在用IL-4培养时会增加表达FcεRⅡ/CD23的细胞数量,并提高这些细胞上FcεRⅡ/CD23的表达水平。FcεRⅡ/CD23的诱导对IL-4具有特异性,因为白细胞介素-1α(IL-1α)、白细胞介素-2(IL-2)、γ干扰素(IFN-γ)、B细胞源性B细胞生长因子(BCGF)和低分子量BCGF均无效。IFN-γ强烈抑制IL-4对FcεRⅡ/CD23的诱导。