为探讨γ干扰素（ＩＦＮ）对胃癌细胞（ＳＧＣ７９０１）肿瘤坏死因子（ＴＮＦ）受体的影响及与肿瘤坏死因子突变体（ＴＮＦｍ）协同抗肿瘤的机制，以１２５ＩＴＮＦｍ为配体，用放射受体分析法研究γＩＦＮ对ＳＧＣ７９０１细胞ＴＮＦ受体表达及与ＴＮＦｍ内化和降解的影响。并用ＭＴＴ法研究γＩＦＮ与ＴＮＦｍ协同抗肿瘤作用。结果：γＩＦＮ使ＳＧＣ７９０１细胞ＴＮＦ受体的数量由０５６×１０－１１ｎｍｏｌ／细胞增至０９４×１０－１１ｎｍｏｌ／细胞，而对受体的亲和力无影响（Ｋｄ为２７８×１０－１１和２６４×１０－１０ｍｏｌ／Ｌ，ｔ＝１２，Ｐ＞０５）；γＩＦＮ可明显增加ＴＮＦｍ内化和降解的绝对数量，而对其比率无影响。γＩＦＮ使ＴＮＦｍ对ＳＧＣ７９０１细胞的最大杀伤率达到９６％（ｔ＝５２，Ｐ＜００１）。提示：γＩＦＮ通过上调ＴＮＦ受体而加强ＴＮＦｍ的体外抗肿瘤作用。 To investigate the effect of IFN-γ on tumor necrosis factor receptor (TNF) receptors in gastric cancer cells (SGC7901) and the synergistic antitumor mechanism with tumor necrosis factor mutant (TNF-m), 125ITNFm Ligands were used to study the effect of γIFN on the expression of TNF receptor and the internalization and degradation of TNFm in SGC7901 cells by radioreceptor assay. MTT assay was used to study the synergistic antitumor effects of γIFN and TNFm. RESULTS: γ  IFN increased the number of TNF receptors in SGC7901 cells from 056×10-11 nmol/cell to 0.94×10-11 nmol/cell, but had no effect on receptor affinity (Kd was 278× 10-11 and 264×10-10 mol/L, t=12, P>05); γIFN can significantly increase the absolute amount of TNFm internalization and degradation without affecting its ratio. . γ  IFN caused TNFm to kill the SGC7901 cells with 96% (t=52, P<001). Tip: γ  IFN enhances the anti-tumor effect of TNFm in vitro by upregulating TNF receptors.