Goedegebuure P S, Segal D M, Braakman E, Vreugdenhil R J, Van Krimpen B A, Van de Griend R J, Bolhuis R L
Department of Immunology, Dr. Daniel den Hoed Cancer Center, Rotterdam, the Netherlands.
J Immunol. 1989 Mar 15;142(6):1797-802.
The requirements for activation of the lytic machinery through CD2 of TCR gamma delta+/CD3+ cells were examined, by utilizing bispecific heteroconjugates containing anti-CD2 mAb cross-linked to anti-DNP. Contrary to the CD2 activation requirements in TCR alpha beta+/CD3+ cells, cytotoxic activity in TCR gamma delta+/CD3+ clones and TCR-/CD3- NK cell clones can be induced by heteroconjugates containing a single anti-CD2 (OKT11.1) mAb. Activation of TCR gamma delta+/CD3+ cells via CD2 is independent of heteroconjugates binding to CD16 (Fc gamma RIII), because heteroconjugates prepared from Fab fragments induced equal levels of lysis. Moreover, anti-CD16 mAb did not inhibit triggering via CD2 in TCR gamma delta+/CD3+ cells. In TCR-/CD3- NK cells, however, induction of cytotoxicity via CD2 is co-dependent on interplay with CD16. Anti-CD3 mAb blocked the anti-CD2 x anti-DNP heteroconjugate-induced cytotoxicity of TCR gamma delta+/CD3+ cells, indicating a functional linkage between CD2 and CD3 on these cells. We conclude that induction of lysis via CD2 shows qualitatively different activation requirements in TCR gamma delta+/CD3+, TCR alpha beta+/CD3+ CTL and TCR-/CD3- NK cells.
通过利用含有与抗二硝基苯（anti-DNP）交联的抗CD2单克隆抗体（mAb）的双特异性异源缀合物，研究了通过TCRγδ⁺/CD3⁺细胞的CD2激活溶解机制的要求。与TCRαβ⁺/CD3⁺细胞中的CD2激活要求相反，含有单一抗CD2（OKT11.1）mAb的异源缀合物可诱导TCRγδ⁺/CD3⁺克隆和TCR⁻/CD3⁻自然杀伤（NK）细胞克隆中的细胞毒性活性。通过CD2激活TCRγδ⁺/CD3⁺细胞独立于异源缀合物与CD16（FcγRIII）的结合，因为由Fab片段制备的异源缀合物诱导相同水平的细胞溶解。此外，抗CD16 mAb不抑制TCRγδ⁺/CD3⁺细胞中通过CD2的触发。然而，在TCR⁻/CD3⁻ NK细胞中，通过CD2诱导细胞毒性共同依赖于与CD16的相互作用。抗CD3 mAb阻断了抗CD2 x抗DNP异源缀合物诱导的TCRγδ⁺/CD3⁺细胞的细胞毒性，表明这些细胞上CD2和CD3之间存在功能联系。我们得出结论，通过CD2诱导溶解在TCRγδ⁺/CD3⁺、TCRαβ⁺/CD3⁺细胞毒性T淋巴细胞（CTL）和TCR⁻/CD3⁻ NK细胞中显示出质的不同的激活要求。
