Klaus G G
Eur J Immunol. 1976 Jun;6(6):389-93. doi: 10.1002/eji.1830060603.
Injection of mice already making antibodies to 2,4-dinitrophenylated (DNP) Ficoll with tolerizing doses of DNP-pneumococcal polysaccharide (DNP-lys-S3) markedly inhibits the secretion of anti-DNP antibodies by IgM antibody-forming cells. The present study shows that the degree of inhibition depends not only on the dose of DNP-lys-S3 but also on the duration of exposure to antigen. DNP-lys-S3 was detectable on the surface of antibody-forming cells at a time when their rate of secretion was unimpaired, thus suggesting that the inhibition involves intracellular events subsequent to the binding of antigen to the cell membrane. The inhibition was reversible if antibody-forming cells were exposed to antigen for 24 h, and then cultured for 18 h in its absence, but became irreversible if the treatment period was extended to 48 h. The relevance of this model of inhibition of lymphocyte function by antigen to possible mechanisms of B cell tolerance is discussed.
向已经对2,4 - 二硝基苯基化(DNP)菲可产生抗体的小鼠注射耐受剂量的DNP - 肺炎球菌多糖(DNP - lys - S3),可显著抑制IgM抗体形成细胞分泌抗DNP抗体。本研究表明,抑制程度不仅取决于DNP - lys - S3的剂量,还取决于抗原暴露的持续时间。在抗体形成细胞的分泌速率未受损害时,可在其表面检测到DNP - lys - S3,这表明抑制涉及抗原与细胞膜结合后的细胞内事件。如果抗体形成细胞暴露于抗原24小时,然后在无抗原的情况下培养18小时,抑制是可逆的,但如果治疗期延长至48小时,抑制则变为不可逆。本文讨论了这种抗原抑制淋巴细胞功能模型与B细胞耐受可能机制的相关性。