Regulation of Fc receptor for IgE (CD23) and class II MHC antigen expression on Burkitt's lymphoma cell lines by human IL-4 and IFN-gamma.
Regulation of Fc receptor for IgE (CD23) and class II MHC antigen expression on Burkitt's lymphoma cell lines by human IL-4 and IFN-gamma.
复制标题
人 IL-4 和 IFN-γ 对伯基特淋巴瘤细胞系上 IgE (CD23) 和 II 类 MHC 抗原表达的 Fc 受体的调节。
作者：
F. Rousset;R. D. W. Malefijt;B. Slierendregt;J. Aubry;J. Bonnefoy;T. Defrance;J. Banchereau;J. D. Vries
研究了rIL-4对Burkitt淋巴瘤（BL）细胞系上IgE的Fc部分的低亲和力受体（FcCR 2/CD 23）和II类MHC抗原的表达的影响。部分BL系含有低百分比的CD 23和HLA-DQ阳性细胞，但几乎所有细胞都表达HLA-DR。IL-4诱导9个BL中7个表达CD 23和II类MHC Ag。孵育48-72小时后观察到最佳的CD 23和II类MHC表达。IL-4对BL细胞系BL 2中CD 23和II类MHC Ag的诱导作用在特异性mRNA水平得到证实。与IL-4孵育6 h后获得HLA-DQ mRNA的显著激活，并在长时间孵育期间逐渐增加。mRNA转录的最大诱导发生在48至72小时后。在48至72 h后也观察到BL 2中HLA-DR和CD 23转录的最佳诱导。CD 23和II类MHC Ag的诱导似乎对IL-4具有特异性，因为rIL-1、rIL-2、rIFN-γ、重组粒细胞-巨噬细胞-CSF和低m.w. B细胞生长因子无效。此外，I类MHC Ag、转铁蛋白受体、CD 38、CD 25、CD 10、CD 20和CD 21的表达不受IL-4的影响。有趣的是，IFN-γ和PGE 2以剂量依赖性方式抑制IL-4诱导的CD 23和II类MHC Ag的膜表达。IFN-γ也完全阻断IL-4诱导的BL 2细胞中CD 23 mRNA的转录，而PGE 2（10（-7）M）具有部分抑制作用。由IL-4诱导的CD 23和II类MHC Ag需要完整的蛋白质合成，如放线菌酮对其的抑制所示。这些结果表明IL-4对CD 23和II类MHC Ag的诱导以协调的方式调节。
The effect of rIL-4 on the expression of low affinity receptor for the Fc part of IgE (Fc epsilon R2/CD23) and class II MHC antigens on Burkitt's lymphoma (BL) cell lines was investigated. Some of the BL lines contained low percentages of CD23 and HLA-DQ-positive cells, but virtually all cells expressed HLA-DR. IL-4 induced CD23 and class II MHC Ag expression on 7 of 9 BL. Optimal CD23 and class II MHC expression was observed after 48-72 h of incubation. Induction of CD23 and class II MHC Ag in the BL cell line BL2 by IL-4 was confirmed at the specific mRNA level. Significant activation of HLA-DQ mRNA was obtained after 6 h of incubation with IL-4 and gradually increased during prolonged incubation. Maximal induction of mRNA transcription occurred after 48 to 72 h. Optimal induction of HLA-DR and CD23 transcription in BL2 was also observed after 48 to 72 h. The induction of CD23 and class II MHC Ag seems to be specific for IL-4, because rIL-1, rIL-2, rIFN-gamma, recombinant granulocyte-macrophage-CSF, and a commercial source of low m.w. B cell growth factor were ineffective. In addition, the expression of class I MHC Ag, the transferrin receptor, CD38, CD25, CD10, CD20, and CD21 were not affected by IL-4. Interestingly, IFN-gamma and PGE2 suppressed the IL-4-induced membrane expression of CD23 and class II MHC Ag in a dose-dependent way. IFN-gamma also blocked IL-4-induced CD23 mRNA transcription in BL2 completely, whereas PGE2 (10(-7) M) was partially inhibitory. The induction of CD23 and class II MHC Ag by IL-4 required intact protein synthesis as shown by its inhibition by cycloheximide. These results indicate that the induction of CD23 and class II MHC Ag by IL-4 is regulated in a coordinated way.