REGULATION OF THE ANTIBODY RESPONSE TO MICROBIAL POLYSACCHARIDE ANTIGENS

几种脂多糖的免疫调节特性 来源于临床分离的铜绿假单胞菌Branhamella 和百日咳波尔德氏菌的能力进行了评估 对III型肺炎球菌抗体应答大小的影响 多糖(SSS-III)，已知在负性和负性调节下 抑制和放大T细胞(Ts和Ta， )。免疫后两天注射脂多糖 导致抗体反应显著增加。是这样的 增强似乎是由于脂蛋白A部分的能力 消除激活TS的负面影响，从而使Ta 功能要得到更充分的表达。相比之下，用内毒素治疗 SSS-III特异性免疫的时间，即在激活之前 TS诱导对SSS-III特异性抗体的显著抑制 反应，这种抑制独立于内毒素的能力 多克隆地激活B细胞，这种活动通常被归因于 脂类脂多糖的一小部分。铜绿假单胞菌内毒素的研究 表明诱导的抑制是T细胞依赖的，并由 内毒素的多糖组分：它似乎是应该的--至少 在一定程度上-以PS的容量来扩展或增加 响应SSS-III而激活的TS前驱体池。这些发现 提示内毒素PS组分增强TS功能的能力 可能在某些革兰氏阴性菌的发病机制中起重要作用 感染。

The immunomodulatory properties of several lipopolysaccharides (LPS) derived from clinical isolates of Pseudomonas aeruginosa, Branhamella catarrhalis, and Bordetella pertussis were evaluated for their capacity to influence the magnitude of the antibody response to type III pneumococcal polysaccharide (SSS-III), which is known to be regulated in a negative and positive manner by suppressor and amplifier T cells (Ts and Ta, respectively). The administration of LPS, two days after immunization result in a significant increase in the antibody response. Such enhancement appears to be due to the ability of the lipid A moiety of LPS to abolish the negative effects of activated Ts, thereby enabling Ta function to be more fully expressed. By contrast, treatment with LPS a the time of immunization with SSS-III-specific i.e., prior to the activation of Ts induces significant suppression of the SSS-III-specific antibody response, such suppression is independent of the capacity of LPS to activate B cells polyclonally, an activity generally attributed to the lipid A fraction of LPS. Studies conducted with LPS of P. aeruginosa indicated that the suppression induced is T-cell dependent and mediated by the polysaccharide (PS) fraction of LPS: it appears to be due - at least in part - to the capacity of PS to expand or increase the size of the precursor pool of Ts, activated in response to SSS-III. These findings suggest that the capacity of the PS fraction of LPS to augment Ts function may play an important role in the pathogenesis of certain gram-negative infections.