Aim To discuss the correlation of the polymorphism of tumor necrosis factor receptor superfamily 1B (TNFRSF1B) in the 196ed gene (T mutation for G) to the inflammation reaction mediated by the macrophage TNF-TNFR2 signaling pathways.Methods Genetic recombination technology was used to bulid eukaryotic expression vector pcDNA6.0-TNFR2196Met and pcDNA6.0-TNFR2196Arg, together with pcDN6.0 being transferred to macrophage by liposome transfection method respectively. In order to establish stable transfection cell lines, blasticidin was used to select them for 4 weeks after transfected 48 h. Digest the macrophages by pancreatic enzyme and divide them into four groups: control group, pcDNA6.0 empty plasmid group, pcDNA6.0-TNFR2196Met group and pcDNA6.0-TNFR2196Arg group. TNFR2, cIAP₁, cIAP₂ mRNA were detected by RT-PCR, the expression of p-JNK, cIAP₁, cIAP₂, TNFR2 and NF-κB were detected by Western blot, the level of sTNFR2, IL-1β and IL-6 in cell supernatant fluid were detected by ELISA.ResultsTNFR2 gene 196Met and 196Arg expression vector were successfully constructed which was verified by enzyme sequencing method. After transfected to marcophages, TNFR2, cIAP₁, cIAP₂, IL-1β, IL-6 and p-JNK expression were increased (P<0.05) in TNFR2196Arg and TNFR2196Met overexpression group compared with the blank control group and empty plasmid group. Each index decreased obviously in mutant TNFR2196Arg cell group compared with TNF2196Met cell group, especially,the reduction of NF-κB activity mediated by TNFR2196Arg was significant. Conclusions Successfully building stable expression TNFR2196Arg and TNFR2196Met vector will lay the foundation for the next inflammation research. The mutation of TNFR2 mediates inflammatory disease through TNF/TNFR2 signaling pathways, which is molecular mechanism of chronic inflammatory disease.