Bakouche O, Gerlier D
Immunology. 1986 Feb;57(2):219-23.
The immunogenicity of Gross virus cell surface antigen (GCSAa) extracted from rat lymphoma cells can be dramatically increased by its presentation into liposomes, probably by mimicking the cell membrane presentation. Induction of an anti-GCSAa secondary antibody response has been found to require the use of liposomes as GCSAa vehicle for both the priming and the boosting immunizations. In order to investigate the sensitivity of highly immune cells to the liposome presentation, immune spleen cells were stimulated in vitro with either soluble GCSAa or GCSAa-liposomes and transferred together with the immunogen into syngeneic animals. Only spleen cells from high responders, which have been immunized twice with GCSAa-liposomes, were able to generate an antibody response in naive recipients after their restimulation with the GCSAa-liposome preparation. Their restimulation with soluble antigen was ineffective unless 10% peritoneal exudate cells (PEC) from naive rats were added during the in vitro incubation. Stimulation with GCSAa-liposomes was further improved by the addition of 10% PEC. Macrophages were found to play a central role in the induction of antibody response in the recipients after stimulation with GCSAa-liposomes. Treatment of immune spleen cells with the macrophage-killing agent leucine methyl ester prior their restimulation in vitro with GCSA-liposomes in the absence of PEC, or depletion of macrophage after their in vitro incubation with this immunogen, completely abolished the induction of anti-GCSAa antibodies in the recipients.
从大鼠淋巴瘤细胞中提取的格罗斯病毒细胞表面抗原(GCSAa),通过将其呈递到脂质体中,免疫原性可能会显著增强,这可能是通过模拟细胞膜呈递实现的。已发现诱导抗GCSAa二级抗体反应需要将脂质体用作GCSAa载体,用于初次免疫和加强免疫。为了研究高免疫细胞对脂质体呈递的敏感性,用可溶性GCSAa或GCSAa-脂质体在体外刺激免疫脾细胞,并将其与免疫原一起转移到同基因动物体内。只有用GCSAa-脂质体免疫过两次的高反应者的脾细胞,在用GCSAa-脂质体制剂再次刺激后,才能在未免疫的受体中产生抗体反应。用可溶性抗原再次刺激无效,除非在体外培养期间加入10%来自未免疫大鼠的腹腔渗出细胞(PEC)。加入10%PEC可进一步增强用GCSAa-脂质体进行的刺激。发现巨噬细胞在用GCSAa-脂质体刺激后,在受体抗体反应的诱导中起核心作用。在用GCSA-脂质体在无PEC的情况下体外再次刺激之前,用巨噬细胞杀伤剂亮氨酸甲酯处理免疫脾细胞,或在用该免疫原进行体外培养后耗尽巨噬细胞,完全消除了受体中抗GCSAa抗体的诱导。