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通过体外分离培养和体内注射ＩＦＮ－γ，研究了巨噬细胞内一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）的诱导合成。体外培养条件下，ＩＦＮ－γ能够诱导小鼠腹腔巨噬细胞合成一氧化氮，与对照组相比有显著差异（Ｐ＜００１）。巨噬细胞内一氧化氮的诱导合成水平同ＩＦＮ－γ的剂量有关。ＴＮＦ－α能够显著增强ＩＦＮ－γ的诱导合成ＮＯ作用。ＩＦＮ－γ在体内可以增强巨噬细胞的一氧化氮合成能力。研究表明，诱导巨噬细胞合成一氧化氮是一种非特异性免疫反应，ＩＦＮ－γ诱导免疫细胞通过Ｌ－精氨酸途径合成一氧化氮有可能是宿主抵抗感染的重要机制。
The induction and synthesis of nitric oxide (NO) in macrophages was studied by in vitro culture and in vivo injection of IFN-γ. Under in vitro culture conditions, IFN-γ induced nitric oxide synthesis in mouse peritoneal macrophages, which was significantly different from the control group (P <001). The level of nitric oxide induced synthesis in macrophages is related to the dose of IFN-γ. TNF-α can significantly enhance IFN-γ-induced NO synthesis. IFN-γ in vivo can enhance macrophage nitric oxide synthesis. Studies have shown that induction of nitric oxide synthesis by macrophages is a nonspecific immune response. IFN-γ-induced immune cells synthesize nitric oxide through the L-arginine pathway may be an important mechanism of host resistance to infection.