CARRIER-PRIMING LEADS TO HAPTEN-SPECIFIC SUPPRESSION
CARRIER-PRIMING LEADS TO HAPTEN-SPECIFIC SUPPRESSION
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DOI：
10.1038/285664a0
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发表时间：
1980-01-01
期刊：
影响因子：
64.8
通讯作者：
HERZENBERG, LA
中科院分区：
文献类型：
--
作者：
HERZENBERG, LA;TOKUHISA, T;HERZENBERG, LA
过去二十年的研究已经确立了1，2‘辅助’T淋巴细胞与‘载体’蛋白结合可增强B淋巴细胞对该载体蛋白上‘半抗原’决定因素的抗体反应。许多工作人员已经证明，来自供者的T细胞以一种常用的载体蛋白--锁孔帽状血蓝蛋白(KLH)激活，可以增强由DNP-KLH刺激的过继受者的B细胞免疫球蛋白G抗二硝基苯基(DNP)反应。因此，我们最近惊讶地发现，在领养转移中，我们通常用作携带者特异性辅助T细胞的供体的KLH3小鼠在受到DNP-KLH3刺激时，抗DNP抗体的产生减少而不是增加。在这里，我们表明，半抗原特异性的抗体产生的调节是导致这种反应失败的原因。也就是说，在DNP-KLH暴露前进行KLH化可减少Ig G抗DNP抗体的产生，而不干扰抗KLH反应或抗DNP记忆B细胞的发育，并且在DNP进一步刺激KLH或无关载体后，Ig G抗DNP的产生保持在低水平。因此，最初对载体蛋白的刺激产生了一种奇怪的折衷动物，在这种动物中，尽管存在正常的抗半抗原记忆和能够支持对半抗原-载体结合物的其他反应的载体特异性帮助，但针对载体上的一种新的半抗原决定簇的IgG抗体的产生保持在最低水平。
Studies over the past two decades have established1,2that ‘helper’ T lymphocytes primed to a ‘carrier’ protein increase B-lymphocyte antibody responses to ‘haptenic’ determinants on the carrier protein. T cells from donors primed with one commonly used carrier protein, keyhole limpet haemocyanin (KLH), have been shown by many workers to augment B-cell IgG anti-dinitrophenyl (DNP) responses in adoptive recipients stimulated with DNP-KLH. Therefore, we were surprised recently to find that the KLH-primed mice we normally use as donors for carrier-specific helper T cells in adoptive transfers3show reduced rather than augmented IgGin situanti-DNP antibody production when stimulated with DNP-KLH. Here we show that hapten-specific regulation of antibody production is responsible for this response failure. That is, that KLH-priming before DNP-KLH exposure reduces the production of IgG anti-DNP antibody without interfering with the anti-KLH response or with the development of anti-DNP memory B cells, and that IgG anti-DNP production remains low after further stimulation with DNP on KLH or an unrelated carrier. Thus initial stimulation with a carrier-protein creates an oddly compromised animal in which IgG antibody production to a ‘new’ haptenic determinant on the carrier is kept minimal despite the presence of normal anti-hapten memory and carrier-specific help capable of supporting other responses to the hapten-carrier conjugate.