Brown P B, Köhler H, Rowley D A
J Immunol. 1975 Aug;115(2):419-24.
BALB/c mice immunized with either the whole vaccine or the C-polysaccharide obtained from the R36A strain of pneumococcus produce antibody to phosphorylcholine. Mice injected i.v. with a single high dose of the C-polysaccharide are specifically unresponsive to immunization to phosphorylcholine for many months and are considered paralyzed. The induction of paralysis does not eliminate cells reactive to phosphorylcholine; however, serum from paralyzed mice specifically suppresses the response of cultures of normal spleen cells to phosphorylcholine. Paralyzed mice have an early low antibody response to phosphorylcholine and to the receptor for phosphorylcholine as indicated by plaque-forming cell assays. The factor or factors present in serum which may suppress cultures, and, by presumption, be responsible for paralysis are complexes of antigen, antibody, and antibody to the receptor for phosphorylcholine.
用全疫苗或从肺炎球菌R36A菌株获得的C多糖免疫的BALB/c小鼠会产生针对磷酸胆碱的抗体。静脉注射单次高剂量C多糖的小鼠在许多个月内对磷酸胆碱免疫产生特异性无反应,被认为处于麻痹状态。麻痹的诱导并没有消除对磷酸胆碱有反应的细胞;然而,麻痹小鼠的血清特异性抑制正常脾细胞培养物对磷酸胆碱的反应。如空斑形成细胞试验所示,麻痹小鼠对磷酸胆碱和磷酸胆碱受体有早期低抗体反应。血清中可能抑制培养物并据推测导致麻痹的一种或多种因子是抗原、抗体和磷酸胆碱受体抗体的复合物。