POTENTIATION OF ANTIBODY-RESPONSES BY SPECIFIC IGM - SPECIFICITY AND THYMUS DEPENDENCY
POTENTIATION OF ANTIBODY-RESPONSES BY SPECIFIC IGM - SPECIFICITY AND THYMUS DEPENDENCY
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DOI：
10.1016/0008-8749(83)90049-7
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发表时间：
1983-01-01
影响因子：
4.3
通讯作者：
LAMON, EW
中科院分区：
文献类型：
--
作者：
COLLISSON, EW;ANDERSSON, B;LAMON, EW
研究了针对免疫原的IgM诱导的抗体应答的调节。当直接抗牛红细胞（ORBC）的IgM与三硝基苯基（TNP）-ORBC一起给予时，随后对载体ORBC的抗体应答以及对半抗原TNP的应答被增强，具有载体特异性的IgG被两种应答抑制。在直接和间接噬斑中都发现了半抗原特异性增强，并且是抗原剂量依赖性的，即，在最低抗原剂量下没有发现增强作用。对2，4-二硝基苯基（DNP）标记的蛋白质的反应被具有半抗原特异性的单克隆IgM增强。在初级和次级反应中都观察到了这种效应。观察到IgM增强发生的一个严格要求。增强所针对的决定簇必须与IgM所针对的决定簇物理连接，无论是半抗原决定簇还是载体决定簇。不相关的IgM-抗原复合物不能增强反应。IgG诱导的抗体反应抑制也有类似的特异性要求。用裸鼠及其正常胸腺同窝出生的小鼠进行的实验表明，IgM增强抗体产生是T细胞依赖性的。被动转移的载体引发的脾细胞与抗原的挑战表明，IgM增强的二次抗体反应是依赖于特定的载体引发的未成熟的T细胞。
Modulation of antibody responses induced by IgM directed against the immunogen was investigated. When IgM directed against ox erythrocytes (ORBC) was given together with trinitrophenyl (TNP)-ORBC, the subsequent antibody response to the carrier, ORBC, as well as the response to the hapten, TNP, was potentiated, IgG with carrier specificity inhibited by both responses. The hapten-specific potentiation was found in both direct and indirect plaques, and was antigen-dose dependent, i.e., no potentiation was found with the lowest antigen doses. The response to 2,4-dinitrophenyl (DNP)-labeled proteins was potentiated by a monoclonal IgM with specificity for the hapten. The effects were observed both in primary and secondary responses. One strict requirement for IgM potentiation to occur was observed. The determinant against which potentiation was achieved had to be physically linked to the determinant against which the IgM was directed, be it hapten or carrier determinants. Irrelevant IgM-antigen complexes were incapable of potentiating the responses. Similar specificity requirements were found for IgG-induced suppression of antibody responses. Experiments with nude mice and their euthymic littermates showed that IgM potentiation of antibody production is T-cell dependent. Passive transfer of carrier-primed spleen cells together with antigen challenge suggests that IgM potentiation of secondary antibody responses is dependent on specific carrier-primed immature T cells.