REGULATION OF THE ANTIBODY RESPONSE TO MICROBIAL POLYSACCHARIDE ANTIGENS

糖化蛋白(GP)，从滑行细菌中分离出来 强生细胞吞噬菌具有多种生物学和免疫学特性 通常归因于脂多糖(LPS)或 革兰氏阴性细菌的内毒素。他们能够(A)激活 70Z/3前B细胞合成IgM，(B)从两者诱导B细胞 内毒素应答和内毒素缺陷品系C3H小鼠的合成 非抗原特异性多克隆免疫球蛋白，(C)诱导巨噬细胞 产生肿瘤坏死因子(TNF)，以及(D)调节 在没有调节性T细胞的情况下的抗体反应。这 发生，尽管GP不含脂质A以及 2-酮-3-脱氧辛糖酸酯，两种常见的成分 细菌内毒素制剂。脂类A的能力来源于 球形红假单胞菌的无毒内毒素阻断能力 毒素--而不是糖蛋白--通过巨噬细胞诱导肿瘤坏死因子，提示糖蛋白 而内毒素可能通过不同的机制和/或细胞表面发挥作用 受体，以引发观察到的影响。

Glycosylated proteins (GP), isolated from the gliding bacterium Cytophaga johnsonae, possess several biological and immunological properties usually attributed to the lipopolysaccharides (LPS) or endotoxins of gram-negative bacteria. They are able to (a) activate 70Z/3 pre-B cells to synthesize IgM, (b) induce B cells from both LPS-responsive and LPS-defective strains of C3H mice to synthesize non-antigen-specific polyclonal immunoglobulin, (c) induce macrophages to produce tumor necrosis factor (TNF), and (d) modulate the magnitude of the antibody response in the absence of regulatory T cells. This occurs, despite the fact that GP are free of lipid A as well as 2-keto-3-deoxyoctonate, two components that are common to all preparations of bacterial LPS. The ability of lipid A derived from the nontoxic LPS of Rhodopseudomonas sphaeroides to block the ability of toxic LPS - but not GP - to induce TNF by macrophages, suggest that GP and LPS may be acting through different mechanisms and/or cell surface receptors to elicit the effects observed.