〔Abstract〕 Objective To observe the expression of TNFR2 in the liver of mice and to explore the relationship between TNFR2 and the immune liver injury induced by trichloroethylene in mice. Methods Twenty-one BALB/c mice from 6 to 8 weeks of age were randomly divided into blank control group(n=5), solvent control group(n=5) and TCE treatment group(n=11). A TCE-sensitized mouse model was established according to the pre-sensitization method of the research group. Twenty-four hours after the last challenge, the skin sensitization response of the mice was scored, and the mice in the TCE group were divided into the TCE-sensitized group and the TCE non-sensitized group. The mice were sacrificed 72 hours after the last challenge, and the blood was collected from the venous plexus of the eye to measure liver function indexes such as alanine aminotransferase(ALT) and aspartate aminotransferase(AST). The liver of the mice was taken out and made into paraffin sections. HE staining was used to observe the pathological features of the liver. Immunohistochemistry method and Western blot method were used to determine the expression of TNF-α and TNFR2 in mouse liver.Real-time fluorescence quantitative PCR method was used to detect the level of TNFR2 gene in mouse liver. Results The sensitization rate of the TCE group was 45.45%(5/11); the serum ALT and AST levels of the TCE-sensitized group were significantly higher than those of the blank control group, solvent control group and TCE unsensitized group, and the difference was statistically significant(P<0.05). HE staining results showed that the blank control group, the solvent control group and the TCE unsensitized group had normal liver cell morphology and even staining. The TCE-sensitized group showed cell swelling and vacuolar degeneration. Immunohistochemical experiments showed that the TCE-sensitized group had a higher expression of TNF-α, a large number of TNFR2 positive expressions could be observed in the TCE-sensitized group compared with other groups, and the difference in scores was statistically significant(P<0.05). Real-time fluorescence PCR results showed that the expression of TNFR2 gene in the TCE-sensitized group was also significantly higher than that in the other groups(P<0.05). Western blot method was used to determine the expression level of TNFR2 protein in the liver of mice, and it was found that the protein expression level of TCE-sensitized group was higher than that of the other three groups(P<0.05). Conclusion The expression of TNFR2 in the liver of TCE-sensitized mice is significantly higher than that of other groups, suggesting that the expression of TNFR2 may be related to the immune liver injury in TCE-sensitized mice.