Abstract: Objective  To explore the role of innate immunity induced by absent in melanoma 2 (AIM2) in the pathogenesis of chronic hepatitis B (CHB). Methods  A total of 70 cases were enrolled in this study, including 47 CHB cases as the experimental group and 23 cases of fatty liver as the controls group. The immunohistochemical method was adopted to detect the expressions of AIM2, Caspase-1, IL-1β and IL-18 in liver tissues. The differences between the two groups were compared with chi-square test, and the correlation was analyzed using spearman test. Results  The positive rate of AIM2 expression in the experimental group (89.3%) was significantly higher than  that in the control group (43.5%) (χ2 = 15.655, P<0.01). In the experimental group, Caspase-1 was positively correlated with AIM2 (rs=0.738, P<0.01); IL-1β and IL-18 were positively correlated with AIM2 (rs=0.527, 0.642, P<0.01). ALT and AST were positively correlated with AIM2 (rs = 0.325, 0.362, P<0.01). The AIM2 expression in the high HBV titers group (HBV-DNA ≥ 1×105 copies/mL) was significantly higher than that in the low HBV titers group (HBV-DNA < 1×105 copies/ml）(χ2= 27.572, P<0.01). Conclusion  In the innate immune response to HBV infection, AIM2 can recognize HBV-DNA, activate Caspase-1 pathways subsequently, release IL-1β and IL-18 inflammatory factors, thus leading to liver inflammatory damages in chronic hepatitis B.

Key words: Absent in melanoma 2, Chronic hepatitis B, Interleukin-1β, Interleukin-18, Caspase-1