Dingemans K P, Pels E, van Dongen G, den Otter W
J Natl Cancer Inst. 1983 Jan;70(1):181-92.
Peritoneal macrophages isolated from intact inbred C57BL/10ScCr mice and from inbred C57BL/10ScCr mice previously immunized with the allogeneic SL2 lymphoma were incubated with SL2 cells with and without antiserum. The mode of interaction of the cells during the first 4 hours was studied ultrastructurally. Normal macrophages interacted with the tumor cells only when antiserum was present. The main feature was a partial enveloping of the tumor cells by thin lamellipodia without any visible cell damage. Immune macrophages without antiserum killed the tumor cells extracellularly by a process of apoptosis and subsequently phagocytized the cell remnants, as described previously. In the presence of antiserum, immune macrophages phagocytized intact tumor cells with very long, slender lamellipodia. Subsequently, the tumor cells underwent intracellular necrosis that seemed to be initiated by the release by the macrophage of complete lysosomes into the phagosome containing the tumor cell. In addition to altering the mode of interaction, antiserum greatly increased the degree of cytotoxicity.
从完整的近交系C57BL/10ScCr小鼠以及先前用同种异体SL2淋巴瘤免疫过的近交系C57BL/10ScCr小鼠中分离出的腹膜巨噬细胞,分别与有抗血清和无抗血清的SL2细胞一起孵育。在最初4小时内,通过超微结构研究了细胞间的相互作用模式。正常巨噬细胞仅在有抗血清存在时才与肿瘤细胞相互作用。主要特征是肿瘤细胞被薄的片状伪足部分包绕,且无任何可见的细胞损伤。如先前所述,无抗血清的免疫巨噬细胞通过凋亡过程在细胞外杀死肿瘤细胞,随后吞噬细胞残骸。在有抗血清存在的情况下,免疫巨噬细胞用非常长且细长的片状伪足吞噬完整的肿瘤细胞。随后,肿瘤细胞发生细胞内坏死,这似乎是由巨噬细胞将完整的溶酶体释放到含有肿瘤细胞的吞噬体中引发的。除了改变相互作用模式外,抗血清还大大增加了细胞毒性程度。