Oshimi K, Oshimi Y, Yamada O, Wada M, Hara T, Mizoguchi H
Department of Medicine, Tokyo Women's Medical College, Japan.
J Immunol. 1990 May 1;144(9):3312-7.
The role of CD3 and CD8 Ag in CD16-mediated CTL triggering was studied in TCR-alpha beta+ and TCR-gamma delta+ granular lymphocytes (GL). In TCR-alpha beta+/CD3+4-8+16+ GL obtained from patients with GL-proliferative disorders, antibody-dependent cellular cytotoxicity was inhibited by anti-CD3 and anti-CD8 mAb. Anti-CD3 mAb also inhibited antibody-dependent cellular cytotoxicity activity of TCR-gamma delta+/CD3+4-8-16+ GL from a patient and that of TCR-gamma delta+/CD3+4-8+/-16+ T cell clones established from patients with proliferating TCR-gamma delta+ GL. In TCR-gamma delta+ T cell clones, cytotoxicity against Fc gamma R+ targets was induced by stimulation of CD16 Ag with anti-CD16 mAb, and such cytotoxicity was also inhibited by anti-CD3 mAb. These results indicate that CD3 and CD8 molecules play a regulatory role in CD16-mediated CTL triggering.
在TCR-αβ⁺和TCR-γδ⁺颗粒淋巴细胞（GL）中研究了CD3和CD8抗原在CD16介导的细胞毒性T淋巴细胞（CTL）触发中的作用。在从GL增殖性疾病患者获得的TCR-αβ⁺/CD3⁺4⁻8⁺16⁺ GL中，抗CD3和抗CD8单克隆抗体抑制了抗体依赖性细胞毒性。抗CD3单克隆抗体也抑制了来自一名患者的TCR-γδ⁺/CD3⁺4⁻8⁻16⁺ GL以及从增殖性TCR-γδ⁺ GL患者建立的TCR-γδ⁺/CD3⁺4⁻8⁺/⁻16⁺ T细胞克隆的抗体依赖性细胞毒性活性。在TCR-γδ⁺ T细胞克隆中，用抗CD16单克隆抗体刺激CD16抗原可诱导对FcγR⁺靶标的细胞毒性，并且这种细胞毒性也被抗CD3单克隆抗体抑制。这些结果表明，CD3和CD8分子在CD16介导的CTL触发中起调节作用。
