Isobe K, Nakashima I
Department of Immunology, Nagoya University School of Medicine, Japan.
Biochem Biophys Res Commun. 1993 Apr 30;192(2):499-504. doi: 10.1006/bbrc.1993.1443.
By the coculture of tumor cells and resident murine peritoneal macrophages, we found that P1HTR tumor cells, which were the subline of P815 mastocytoma, stimulated syngeneic or allogeneic peritoneal macrophages to produce nitric oxide. This nitric oxide in turn kills P1HTR target cells. The cytotoxicity and nitric oxide production were completely abolished by the addition of L-arginine homologue NG-monomethyl-L-arginine. The original P815 tumor cells had only weak activity to stimulate macrophages to produce nitric oxide and were weekly killed by coculture of P815 and resident macrophages. Macrophage cell line, RAW264-7, was also stimulated to produce nitric oxide by P1HTR cells. The ability to stimulate macrophages to produce nitric oxide resided on the membranous fragment of P1HTR cells.
通过肿瘤细胞与小鼠腹膜常驻巨噬细胞的共培养，我们发现P1HTR肿瘤细胞（P815肥大细胞瘤的亚系）可刺激同基因或异基因腹膜巨噬细胞产生一氧化氮。反过来，这种一氧化氮会杀死P1HTR靶细胞。添加L-精氨酸同系物NG-单甲基-L-精氨酸后，细胞毒性和一氧化氮的产生完全被消除。原始的P815肿瘤细胞刺激巨噬细胞产生一氧化氮的活性较弱，并且在P815与常驻巨噬细胞共培养时被轻度杀伤。巨噬细胞系RAW264-7也被P1HTR细胞刺激产生一氧化氮。刺激巨噬细胞产生一氧化氮的能力存在于P1HTR细胞的膜片段上。
