Elkins K L, Stashak P W, Baker P J
Laboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
Infect Immun. 1987 Dec;55(12):3085-92. doi: 10.1128/iai.55.12.3085-3092.1987.
Pretreatment (priming) of BALB/c mice with a low (subimmunogenic) dose of Escherichia coli O113 lipopolysaccharide (LPS) generates immunological memory 7 to 30 days later; the direct (immunoglobulin M) plaque-forming cell (PFC) responses produced after subsequent immunization with an optimal dose are 4 to 20 times greater than those of unprimed mice. By contrast, priming with a low dose of E. coli O55 LPS, followed by immunization with an optimally immunogenic dose 2 to 30 days later, resulted in a significantly reduced antibody response. Similar results were obtained with Serratia marcescens LPS. Dose-response studies indicated that such unresponsiveness is antigen specific and could be induced with subimmunogenic amounts of LPS. Priming reduced the magnitude of the PFC response to all immunizing doses of LPS tested. Unresponsiveness is not due to (i) an alteration in the time course of the PFC response or to (ii) a change in the isotype of the anti-LPS antibody produced after priming and immunization.
用低剂量(亚免疫原性)的大肠杆菌O113脂多糖(LPS)对BALB/c小鼠进行预处理(致敏),7至30天后会产生免疫记忆;随后用最佳剂量免疫后产生的直接(免疫球蛋白M)噬斑形成细胞(PFC)反应比未致敏小鼠的反应大4至20倍。相比之下,用低剂量的大肠杆菌O55 LPS致敏,然后在2至30天后用最佳免疫原性剂量进行免疫,导致抗体反应显著降低。粘质沙雷氏菌LPS也得到了类似的结果。剂量反应研究表明,这种无反应性是抗原特异性的,并且可以用亚免疫原性量的LPS诱导产生。致敏降低了对所有测试LPS免疫剂量的PFC反应强度。无反应性并非由于(i)PFC反应时间进程的改变,也不是由于(ii)致敏和免疫后产生的抗LPS抗体的同种型变化。