Levy R B, Dower S K, Shearer G M, Segal D M
J Exp Med. 1984 May 1;159(5):1464-72. doi: 10.1084/jem.159.5.1464.
Several anti-H-2Kk but not anti-H-2Dd monoclonal antibodies (mAb) exhibited enhanced binding to B10.A murine spleen cells after modification of the cells with trinitrobenzene sulfonate (TNBS). The number of antibody molecules bound to TNP-modified B10.A spleen cells increased by a factor of two or more. The same anti-2Kk mAb that exhibited enhanced binding to modified B10.A cells did not bind to unmodified C57BL/10 spleen cells, as expected, but did bind to TNP-modified C57BL/10 spleen cells. This TNP-dependent binding was not a result of cross-reactions with cell surface TNP groups nor with Fc receptors. TNP modification of a variant cell line that does not express class I H-2 products did not result in enhanced binding by these mAb. These findings can account for preferential recognition of TNP-Kk by B10.A and B10.BR CTL, and also for cross-reactive lysis by C57BL/10 CTL stimulated by C57BL/10-TNP against unmodified H-2Kk targets.
在用三硝基苯磺酸(TNBS)修饰细胞后,几种抗H-2Kk单克隆抗体(mAb)而非抗H-2Dd单克隆抗体与B10.A小鼠脾细胞的结合增强。与经三硝基苯(TNP)修饰的B10.A脾细胞结合的抗体分子数量增加了两倍或更多。正如预期的那样,与修饰后的B10.A细胞结合增强的相同抗2Kk单克隆抗体不与未修饰的C57BL/10脾细胞结合,但确实与经TNP修饰的C57BL/10脾细胞结合。这种TNP依赖性结合不是与细胞表面TNP基团或Fc受体交叉反应的结果。对不表达I类H-2产物的变异细胞系进行TNP修饰,不会导致这些单克隆抗体的结合增强。这些发现可以解释B10.A和B10.BR细胞毒性T淋巴细胞(CTL)对TNP-Kk的优先识别,以及C57BL/10-TNP刺激的C57BL/10 CTL对未修饰的H-2Kk靶标的交叉反应性裂解。