Allogeneic mixed lymphocyte reactions in humans: pretreatment of either the stimulator or the responder cell population with monoclonal anti-Ia antibodies leads to an inhibition of cell proliferation.

Allogeneic mixed lymphocyte reactions in humans: pretreatment of either the stimulator or the responder cell population with monoclonal anti-Ia antibodies leads to an inhibition of cell proliferation.
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人类同种异体混合淋巴细胞反应:用单克隆抗 Ia 抗体预处理刺激细胞或应答细胞群会导致细胞增殖受到抑制。

DOI:
10.4049/jimmunol.127.6.2438
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发表时间:
1981
影响因子:
4.4
通讯作者:
J. Cerottini
J. Cerottini
中科院分区:
医学2区
文献类型:
--
作者:
R. Accolla;A. Moretta;J. Cerottini

文献摘要

被引文献

相似文献

我们分析了2个杂交瘤单克隆抗体(Mab),D1-12和D4-22,与人类Ia分子的共同决定簇的特异性,对混合淋巴细胞培养(MLC)的反应。结果表明,在培养开始后第3天加入2种Mab中的任一种完全抑制了MLC中产生的增殖反应。由于本研究中使用的2种Mab识别的抗原决定簇已被证明属于不同的Ia分子,因此在含有此类Mab的MLC中观察到的抑制作用似乎不能简单地通过Ia分子对刺激细胞群的掩蔽来解释。与其他研究者先前的研究一致,用溶细胞性D1-12 Mab加补体处理白细胞群体强烈降低了其在MLC中的刺激能力。更重要的是,这种治疗还降低了白细胞群体在MLC中响应的能力。在后一种情况下,抑制作用似乎是针对T细胞的,因为用D1-12加补体处理的高度纯化的E-玫瑰花结细胞在MLC中不能应答。这些结果的可能影响进行了讨论。
We analyzed the effect of 2 hybridoma monoclonal antibodies (Mab), D1-12 and D4-22, with specificity for common determinants of human Ia molecules, on the mixed lymphocyte culture (MLC) response. The results show that addition of either of the 2 Mab as late as day 3 after the onset of the culture completely inhibits the proliferative response generated in MLC. Because the antigenic determinants recognized by the 2 Mab that were used in this study have been shown to belong to distinct Ia molecules, it appears the inhibitory effect observed in MLC containing such Mabs cannot be explained simply by the masking of Ia molecules on the stimulator cell population. In agreement with previous studies by other investigators, treatment of a leukocyte population with the cytolytic D1-12 Mab plus complement strongly reduced its ability to stimulate in MLC. More importantly such a treatment also decreased the ability of a leukocyte population to respond in MLC. In the latter case, the inhibitory effect appears to be directed against T cells since highly purified E-rosetting cells treated with D1-12 plus complement were unable to respond in MLC. The possible implications of these results are discussed.