Gresser I, Maury C, Kaido T, Bandu M T, Tovey M G, Maunoury M T, Fantuzzi L, Gessani S, Greco G, Belardelli F
Laboratory of Viral Oncology (UPR CNRS 9045), Institut de Recherches sur le Cancer/IFC1, Villejuif, France.
Int J Cancer. 1995 Nov 27;63(5):726-31. doi: 10.1002/ijc.2910630520.
Adoptive transfer of splenic T lymphocytes from DBA/2 mice immunized against Friend erythroleukemia cells (FLC) inhibited the development of visceral metastases and increased the survival time of DBA/2 mice challenged i.v. with parental FLC 24 hr to 2 months later. Immune spleen cells were ineffective in mice pre-treated with potent neutralizing antibody to mouse IFN alpha/beta (but not to IFN gamma), demonstrating the essential participation of endogenous IFN alpha/beta in the inhibitory action of immune T lymphocytes against FLC metastases. These findings suggest that the reported inability of immune T lymphocytes to exert an anti-FLC effect in immunodeficient DBA/2 mutant beige (bg/bg) mice (unless these mice had also been treated with IFN alpha/beta), may have been due to lower levels of endogenous IFN alpha/beta in DBA/2 bg/bg mice than in normal DBA/2+/bg mice. Experimental results in support of this hypothesis are presented.
将经抗Friend红白血病细胞(FLC)免疫的DBA/2小鼠的脾T淋巴细胞进行过继转移,可抑制内脏转移的发生,并延长在静脉注射亲代FLC 24小时至2个月后受到攻击的DBA/2小鼠的存活时间。在用针对小鼠IFNα/β(而非IFNγ)的强效中和抗体预处理的小鼠中,免疫脾细胞无效,这表明内源性IFNα/β在免疫T淋巴细胞对FLC转移的抑制作用中起重要作用。这些发现表明,有报道称免疫T淋巴细胞在免疫缺陷的DBA/2突变米色(bg/bg)小鼠中无法发挥抗FLC作用(除非这些小鼠也接受了IFNα/β治疗),这可能是由于DBA/2 bg/bg小鼠中的内源性IFNα/β水平低于正常DBA/2+/bg小鼠。本文展示了支持这一假设的实验结果。