Hirohata S, Inoue T, Miyamoto T
Department of Medicine and Physical Therapy, University of Tokyo School of Medicine.
Arerugi. 1990 Feb;39(2 Pt 1):82-9.
The roles of T cells in in vitro IgM-RF production were examined utilizing two different polyclonal B cell stimulators, Staphylococcus aureus Cowan I (SA) and immobilized mAb to the CD3 molecular complexes (64.1). In cultures stimulated with SA, T4 cells alone but not T8 cells alone could support IgM-RF production. This function of T4 cells could be replaced by IL2 alone or factors generated from mitogen activated T cells (TF). Moreover, when IL2 was supplemented to the cultures, T8 cells as well as T4 cells enhanced the IgM-RF production. Treatment of the T cell subsets with mitomycin C decreased or abrogated the helper function along with a decrease in IL2 production by the T cell subsets in SA stimulated cultures. By contrast, in cultures stimulated with immobilized anti-CD3, T4 cells that had been treated with mitomycin C could induce production of large amounts of IgM-RF, whereas control T4 cells as well as control T8 cells suppressed IgM-RF production. These results indicate that the regulatory functions of T cells in IgM-RF production might be different depending upon the nature of stimulation signals.
利用两种不同的多克隆B细胞刺激剂——金黄色葡萄球菌考恩I型(SA)和针对CD3分子复合物的固定化单克隆抗体(64.1),研究了T细胞在体外IgM类风湿因子(IgM-RF)产生中的作用。在用SA刺激的培养物中,单独的T4细胞而非单独的T8细胞能够支持IgM-RF的产生。T4细胞的这一功能可被单独的白细胞介素2(IL2)或有丝分裂原激活的T细胞产生的因子(TF)所替代。此外,当向培养物中添加IL2时,T8细胞以及T4细胞均增强了IgM-RF的产生。在用丝裂霉素C处理T细胞亚群后,SA刺激的培养物中T细胞亚群的辅助功能降低或消除,同时IL2的产生也减少。相比之下,在用固定化抗CD3刺激的培养物中,经丝裂霉素C处理的T4细胞能够诱导产生大量IgM-RF,而对照T4细胞以及对照T8细胞则抑制IgM-RF的产生。这些结果表明,T细胞在IgM-RF产生中的调节功能可能因刺激信号的性质而异。