Dennert G, Hatlen L E
J Immunol. 1975 Jun;114(6):1705-12.
Techniques are reported for the induction and assay of cytotoxic effector cells capable of specifically lysing hapten-coupled EL4 leukemia targets. It is shown that EL4 cells survive coupling with TNP-sulfonic acid and retain the hapten on their cell surface for a prolonged period of time. Although TNP-EL4 cells are readily lysed by anti-TNP serum in a complement-mediated reaction, they are inefficiently killed in an antibody-dependent cell-mediated reaction. Cytotoxic effector cells, able to lyse TNP-EL4 targets, are induced when C57BL/6 spleen H-2-b cells are cultured with the following cell types which have been coupled with TNP: 1) ALLOGENEIC P815 tumor cells (H-2-d), 2) syngeneic EL4 tumor cells, 3) allogeneic BALB/c spleen cells (H-2-d), 4) syngeneic C57BL/6 spleen cells. Further experiments show that TNP-coupled xenogeneic chicken erythrocytes, which by themselves are unable to induce cytotoxic effectors, are capable of doing so if uncoupled P815 cells are present simultaneously. On the basis of these findings, it can be hypothesized that two stimuli are required for induction of these cytotoxic effector cells--one provided by the hapten, and the other by the P815 cell. Treatment of cytotoxic spleen cells induced by hapten-coupled allogeneic tumor cells with anti-Thy-1 serum and complement abrogates their cytotoxicity, indicating that T cells play a central role in the cytotoxic reaction. TNP-coupled erythrocytes do not serve as targets for these cytotoxic T cells, but do cause competitive inhibition of TNP-EL4 when added to the reaction mixture at high ratios. However, because the inhibition is relatively low, and because no such inhibition can be demonstrated with TNP-lysine, it is concluded that the receptor on the cytotoxic effector cell has a low affinity for hapten. This low affinity could be due to the receptor recognizing an antigen comprising mouse cell surface antigen in addition to the TNP moiety. Supporting this interpretation is the finding that TNP-EL4 cells competitively inhibit cytotoxicity much more efficiently than TNP-CRBC and that even uncoupled EL4 cells inhibit to some extent.
本文报道了诱导和检测能够特异性裂解半抗原偶联的EL4白血病靶细胞的细胞毒性效应细胞的技术。结果表明,EL4细胞与TNP-磺酸偶联后仍能存活,并在其细胞表面长时间保留半抗原。虽然TNP-EL4细胞在补体介导的反应中很容易被抗TNP血清裂解,但在抗体依赖性细胞介导的反应中它们被低效杀伤。当C57BL/6脾H-2-b细胞与以下已与TNP偶联的细胞类型共培养时,可诱导出能够裂解TNP-EL4靶细胞的细胞毒性效应细胞:1)同种异体P815肿瘤细胞(H-2-d),2)同基因EL4肿瘤细胞,3)同种异体BALB/c脾细胞(H-2-d),4)同基因C57BL/6脾细胞。进一步的实验表明,TNP偶联的异种鸡红细胞本身不能诱导细胞毒性效应细胞,但如果同时存在未偶联的P815细胞,则能够诱导。基于这些发现,可以推测诱导这些细胞毒性效应细胞需要两种刺激——一种由半抗原提供,另一种由P815细胞提供。用抗Thy-1血清和补体处理由半抗原偶联的同种异体肿瘤细胞诱导的细胞毒性脾细胞,可消除其细胞毒性,表明T细胞在细胞毒性反应中起核心作用。TNP偶联的红细胞不是这些细胞毒性T细胞的靶细胞,但当以高比例加入反应混合物时,会对TNP-EL4产生竞争性抑制。然而,由于抑制作用相对较低,且用TNP-赖氨酸未观察到这种抑制作用,因此得出结论,细胞毒性效应细胞上的受体对半抗原有低亲和力。这种低亲和力可能是由于该受体除了识别TNP部分外,还识别包含小鼠细胞表面抗原的抗原。支持这一解释的发现是,TNP-EL4细胞比TNP-CRBC更有效地竞争性抑制细胞毒性,甚至未偶联EL4细胞也有一定程度的抑制作用。