Nakano M, Uchiyama T, Tanabe M J, Saito K
Jpn J Microbiol. 1975 Apr;19(2):141-8. doi: 10.1111/j.1348-0421.1975.tb00860.x.
Mechanisms of nonspecific elicitation of anti-sheep erythrocyte (SRBC) hemolytic antibody plaqueforming cells (PFC) in mouse spleens with an injection of bacterial endotoxin (lipopolysaccharide (LPS)) were studied in comparison with the genesis of naturally occurring "background" PFC in normal mouse spleens and of rapidly arising PFC in mouse spleens after immunization with SRBC. The cytokinetic pattern of anti-SRBC PFC response after an injection of LPS was quite different from that of the response elicited after immunization with SRBC. In addition, even though LPS nonspecifically elicited anti-SRBC PFC response in mice, LPS could not confer any immunological memory on mouse immunocytess for a "secondary-type" anti-SRBC PFC response to restimulation with LPS or SRBC. The administration of rabbit anti-mouse thymocyte immunoglobulin or anti-SRBC antiserum in mice markedly suppressed the PFC response after immunization with SRBC, but did not do so after stimulation with LPS. Neonatally thymectomized mice could still respond to stimulation with LPS, producing anti-SRBC PFC in their spleens. Injections of actinomycin D or cyclophosphamide into mice resulted in obvious reductions of the PFC responses elicited by either LPS or SRBC. However, injections of these immunosuppressive antisera or drugs did not affect the number of anti-SRBC PFC in normal mouse spleens. These results suggest that the genesis of anti-SRBC PFC developed under different conditions, i.e., background PFC, LPS-stimulated PFC, and antigen-stimulated PFC, are quite different from each other, and that the nonspecific elicitation of anti-SRBC PFC by LPS does not require the helper function of T lymphocytes. No obvious difference, however, was observed in the time of ontogenic maturation among these three different anti-SRBC PFC in the mouse spleens judging from when they were first manifested after birth.
通过注射细菌内毒素(脂多糖(LPS))来非特异性诱导小鼠脾脏中抗绵羊红细胞(SRBC)溶血抗体空斑形成细胞(PFC)的机制,与正常小鼠脾脏中自然产生的“背景”PFC以及用SRBC免疫后小鼠脾脏中快速产生的PFC的产生机制进行了比较研究。注射LPS后抗SRBC PFC反应的细胞动力学模式与用SRBC免疫后引发的反应模式有很大不同。此外,尽管LPS能在小鼠中非特异性诱导抗SRBC PFC反应,但LPS不能赋予小鼠免疫细胞任何免疫记忆,使其对LPS或SRBC再刺激产生“二次型”抗SRBC PFC反应。给小鼠注射兔抗小鼠胸腺细胞免疫球蛋白或抗SRBC抗血清可显著抑制用SRBC免疫后的PFC反应,但对LPS刺激后的反应则无此作用。新生期胸腺切除的小鼠仍能对LPS刺激产生反应,在其脾脏中产生抗SRBC PFC。给小鼠注射放线菌素D或环磷酰胺会导致LPS或SRBC引发的PFC反应明显减少。然而,注射这些免疫抑制抗血清或药物并不影响正常小鼠脾脏中抗SRBC PFC的数量。这些结果表明,在不同条件下产生的抗SRBC PFC,即背景PFC、LPS刺激的PFC和抗原刺激的PFC,彼此之间有很大差异,并且LPS非特异性诱导抗SRBC PFC不需要T淋巴细胞的辅助功能。然而,从出生后首次出现的时间判断,在小鼠脾脏中这三种不同的抗SRBC PFC在个体发育成熟时间上未观察到明显差异。