Yoon H J, Aprile J A, Loughran T P
Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.
Cell Immunol. 1990 Dec;131(2):404-8. doi: 10.1016/0008-8749(90)90265-s.
We studied the role of Fc receptors and interleukin-2 (IL-2) receptor subunits in anti-CD3 monoclonal antibody (MAb)-mediated cytotoxicity of CD3+ leukemic large granular lymphocytes (LGL). Peripheral blood mononuclear cells from four patients with CD3+ LGL leukemia were cultured with 1 microgram/ml of anti-CD3 MAb. Anti-CD3 MAb-mediated cytotoxicity was not inhibited when K562 target cells were preincubated with heat-aggregated human IgG, suggesting that binding of the effector cell-bound anti-CD3 MAb to Fc receptors of target was not involved in cytotoxicity. Induction of cytotoxicity was not blocked by the addition of either anti-p55 or anti-p75 IL-2 receptor MAbs. These results show that the induction of cytotoxicity by anti-CD3 MAb is not mediated through IL-2 receptor subunits in CD3+ leukemic LGL.
我们研究了Fc受体和白细胞介素-2（IL-2）受体亚基在抗CD3单克隆抗体（MAb）介导的CD3 +白血病大颗粒淋巴细胞（LGL）细胞毒性中的作用。将来自4例CD3 + LGL白血病患者的外周血单个核细胞与1微克/毫升的抗CD3 MAb一起培养。当K562靶细胞与热聚集的人IgG预孵育时，抗CD3 MAb介导的细胞毒性未受抑制，这表明效应细胞结合的抗CD3 MAb与靶细胞的Fc受体结合不参与细胞毒性。添加抗p55或抗p75 IL-2受体MAb均未阻断细胞毒性的诱导。这些结果表明，抗CD3 MAb诱导的细胞毒性不是通过CD3 +白血病LGL中的IL-2受体亚基介导的。
