Shanahan F, Brogan M D, Newman W, Targan S R
J Immunol. 1986 Jul 15;137(2):723-6.
The monoclonal antibody 13.3 specifically blocks the trigger process of the NK-K562 cytolytic sequence at a post-binding effector cell level. This antibody was used to define differences in the lytic trigger processes of NK and other mechanisms of K562 lysis. Monoclonal antibody 13.3 inhibited lysis of K562 target cells by freshly isolated peripheral blood lymphocytes (PBL) and purified large granular lymphocytes (LGL), but had no inhibitory effect on antibody-dependent cell-mediated cytotoxicity to K562 by these effectors. Lectin-dependent cellular cytotoxicity (LDCC) to this target cell was also unresponsive to 13.3. The 13.3-induced inhibition of NK-K562 lytic activity persisted when PBL were activated in culture with interleukin 2 (IL 2) for periods up to 48 hr. After 48 hr of culture, the degree of inhibition diminished progressively in medium containing fetal calf serum but not in medium containing autologous serum. This 13.3-unresponsive lytic activity in cultured PBL could be attributed to more than one cell type and was present in both the LGL and Fc gamma receptor-depleted T cell fraction. Thus, K562 lysis by freshly isolated human lymphocytes via NK, K, and LDCC mechanisms is characterized by heterogeneity of the post-binding effector cell trigger mechanism. K562 lysis by lymphocytes cultured with IL 2 is similarly heterogeneous.
单克隆抗体13.3在结合后效应细胞水平特异性阻断NK-K562溶细胞序列的触发过程。该抗体用于确定NK的溶细胞触发过程与K562其他裂解机制之间的差异。单克隆抗体13.3抑制新鲜分离的外周血淋巴细胞(PBL)和纯化的大颗粒淋巴细胞(LGL)对K562靶细胞的裂解,但对这些效应细胞对K562的抗体依赖性细胞介导的细胞毒性没有抑制作用。对该靶细胞的凝集素依赖性细胞毒性(LDCC)对13.3也无反应。当用白细胞介素2(IL-2)在培养中激活PBL长达48小时时,13.3诱导的对NK-K562溶细胞活性的抑制作用持续存在。培养48小时后,在含有胎牛血清的培养基中抑制程度逐渐降低,但在含有自体血清的培养基中则不然。培养的PBL中这种对13.3无反应的溶细胞活性可归因于不止一种细胞类型,并且存在于LGL和Fcγ受体缺失的T细胞部分中。因此,新鲜分离的人淋巴细胞通过NK、K和LDCC机制对K562的裂解,其特征在于结合后效应细胞触发机制的异质性。用IL-2培养的淋巴细胞对K562的裂解同样具有异质性。