Kishimoto T, Ishizaka K
J Immunol. 1975 Feb;114(2 Pt 1):585-91.
Attempts were made to induce antibody response of hapten-primed cells by stimulation with anti-immunoglobulin (Ig) antibody and cellfree supernatant (CFS) which contained nonspecific enhancing factor. Mesenteric lymph node cells were obtained from rabbits which were primed with dinitrophenylated ragweed antigen (DNP-Rag), and the primed cells were incubated in vitro with either anti-rabbit gamma-chain or anti-Fab antibody for 24 hr. After washing, the cells were cultured in CFS which was obtained from the culture of DNP-Ascaris (DNP-Asc)-primed lymph node cells with free carrier (Asc). The results showed that hapten-primed cells were triggered for IgG anti-DNP antibody response by the two reagents, i.e., anti-Ig antibody and CFS, both which did not share any antigenic specificity with the priming antigen (DNP-Rag). Neither anti-Ig alone nor CFS alone induced anti-hapten antibody response. Anti-Ig and CFS triggered not only hapten-primed B cells but also the other IgG-bearing (B) cells for IgG synthesis. Lymph node cells of umprimed animals were activated for IgG synthesis by the stimulation with anti-Ig followed by culture in CFS. Evidence was obtained that anti-Ig antibody has to be divalent for the activation of B cells. Stimulation of DNP-primed cells with the F(ab')2 fragment of the antibody and CFS-induced anti-hapten antibody response, whereas the Fag' fragment of the anti-Ig plus CFS failed to do so. The results suggested that bridging of cell-surface Ig receptors by multivalent ligand is the initial step of B cell activation. Another evidence for the activation of hapten-primed B cells by anti-Ig was obtained by supplemental immunization of DNP-Asc-primed animals with the Fc fragment of goat IgG. Stimulation of mesenteric lymph node cells from these animals with goat anti-rabbit-Ig alone (no CFS) resulted in the formation of anti-DNP IgG antibody. The results indicated that lymphocytes primed for goat IgG collaborated with DNP-primed IgG-B cells when the lymph node cells were stimulated with goat anti-Ig.
尝试通过用抗免疫球蛋白（Ig）抗体和含有非特异性增强因子的无细胞上清液（CFS）刺激来诱导半抗原致敏细胞的抗体反应。从用二硝基苯基化豚草抗原（DNP-Rag）致敏的兔子中获取肠系膜淋巴结细胞，并将致敏细胞与抗兔γ链或抗Fab抗体在体外孵育24小时。洗涤后，将细胞在CFS中培养，该CFS是从用游离载体（蛔虫抗原，Asc）致敏的DNP-蛔虫（DNP-Asc）淋巴结细胞培养物中获得的。结果表明，抗Ig抗体和CFS这两种试剂触发了半抗原致敏细胞产生IgG抗DNP抗体反应，而这两种试剂与致敏抗原（DNP-Rag）均无任何抗原特异性。单独的抗Ig抗体或单独的CFS均未诱导抗半抗原抗体反应。抗Ig抗体和CFS不仅触发了半抗原致敏的B细胞，还触发了其他携带IgG的（B）细胞进行IgG合成。未致敏动物的淋巴结细胞通过抗Ig刺激后再在CFS中培养而被激活进行IgG合成。有证据表明，抗Ig抗体必须为二价才能激活B细胞。用抗体的F(ab')2片段和CFS刺激DNP致敏细胞可诱导抗半抗原抗体反应，而抗Ig的Fag'片段加CFS则无法诱导。结果表明，多价配体桥接细胞表面Ig受体是B细胞激活的起始步骤。通过用山羊IgG的Fc片段对DNP-Asc致敏动物进行补充免疫，获得了抗Ig激活半抗原致敏B细胞的另一个证据。仅用山羊抗兔Ig（无CFS）刺激这些动物的肠系膜淋巴结细胞，导致形成抗DNP IgG抗体。结果表明，当淋巴结细胞用山羊抗Ig刺激时，对山羊IgG致敏的淋巴细胞与DNP致敏的IgG-B细胞协同作用。
