Tanabe M J, Saito K
Jpn J Microbiol. 1975 Aug;19(4):299-307. doi: 10.1111/j.1348-0421.1975.tb00883.x.
An attempt was made to determine if there is any common mechanism in the enhanced antibody response caused either by injection of adjuvant, such as bacterial endotoxin (LPS) and complexed poly-nucleotides, or by secondary antigenic stimulation. LPS inoculated in mice 4 days before injection of sheep red cells (SRBC) and polyA:U invalidated the adjuvant effect of polyA:U injected together with SRBC, and the hemolysin plaque-forming cell (PFC) response of such mice was similar to that of the mice which received SRBC alone. When mice primed with SRBC 24 days in advance were injected with LPS and 4 days later re-stimulated with SRBC, their PFC response to the secondary stimulation was suppressed to less than one tenth of the normal secondary PFC response. The suppressive effect of LPS on the secondary antibody response was abolished if the serum collected from mice injected with LPS was given to the primed and LPS-injected mice at the time of the secondary antigenic stimulation. From these results we discussed the possibility that some common mediator might play a role in the enhanced antibody response elicited by either adjuvant injection or secondary injection of antigen.
研究人员试图确定,注射佐剂(如细菌内毒素(LPS)和复合多核苷酸)或二次抗原刺激所引起的抗体反应增强中,是否存在任何共同机制。在注射绵羊红细胞(SRBC)前4天给小鼠接种LPS,以及polyA:U,会使与SRBC一起注射的polyA:U的佐剂效应失效,并且此类小鼠的溶血素空斑形成细胞(PFC)反应与仅接受SRBC的小鼠相似。当预先用SRBC致敏24天的小鼠注射LPS,4天后再次用SRBC刺激时,它们对二次刺激的PFC反应被抑制至正常二次PFC反应的十分之一以下。如果在二次抗原刺激时,将注射LPS的小鼠所采集的血清给予致敏且注射了LPS的小鼠,LPS对二次抗体反应的抑制作用就会被消除。基于这些结果,我们探讨了某种共同介质可能在佐剂注射或抗原二次注射所引发的抗体反应增强中发挥作用的可能性。