Ramirez R, Carracedo J, Mooney N, Charron D
Unidad de Investigación, Hospital Universitario Reina Sofia, Cordoba, Spain.
Cell Immunol. 1993 Dec;152(2):522-9. doi: 10.1006/cimm.1993.1309.
We have studied the role of LFA-1 antigens in human B lymphocyte aggregation, proliferation, and Ig production induced by a short stimulation via class II antigens. Cell stimulation with either bacterial superantigens or anti-DR mAbs rapidly induced homotypic cell aggregation. In response to IL-4, an increase in cell proliferation and Ig production was observed only when aggregation preceded addition of IL-4. The involvement of LFA-1 molecules in class II-induced aggregation was supported as LFA-1-deficient cells or B cells incubated with anti-LFA-1/ICAM-1 mAbs failed to aggregate after stimulation. The association between aggregation and subsequent Ig production and proliferation was further supported as, after IL-4 stimulation, in both LFA-1-deficient cells and B cells incubated with anti-LFA-1 mAbs, class II-mediated signals failed to increase Ig production or cell proliferation. These data suggest that in class II-stimulated cells, LFA-1-dependent aggregation has a major role in IL-4-dependent Ig production and proliferation of B cells.
我们研究了淋巴细胞功能相关抗原-1(LFA-1)抗原在经由Ⅱ类抗原短期刺激所诱导的人B淋巴细胞聚集、增殖及免疫球蛋白(Ig)产生过程中的作用。用细菌超抗原或抗DR单克隆抗体刺激细胞可迅速诱导同型细胞聚集。在白细胞介素-4(IL-4)作用下,仅当聚集先于IL-4添加时,才观察到细胞增殖及Ig产生增加。LFA-1分子参与Ⅱ类抗原诱导的聚集这一观点得到了支持,因为LFA-1缺陷细胞或与抗LFA-1/细胞间黏附分子-1(ICAM-1)单克隆抗体孵育的B细胞在刺激后未能聚集。聚集与随后的Ig产生及增殖之间的关联得到了进一步支持,因为在IL-4刺激后,在LFA-1缺陷细胞及与抗LFA-1单克隆抗体孵育的B细胞中,Ⅱ类抗原介导的信号均未能增加Ig产生或细胞增殖。这些数据表明,在Ⅱ类抗原刺激的细胞中,依赖LFA-1的聚集在B细胞依赖IL-4的Ig产生及增殖中起主要作用。