BACKGROUND:Studies have found that liver cels can synthesize insulin after giving pancreatic and duodenal homeobox 1 (PDX1) gene. Anti-CD20 monoclonal antibody can inhibit the immune reaction of insulin-producing liver cels, but the mechanism is unclear. OBJECTIVE:To observe the influence of interleukin-10 gene on liver cels and liver PDX1 expression in nonobese diabetic mice after interfered by adenovirus vector-mediated murine interleukin-10 and anti-CD20 monoclonal antibody. METHOD:Forty nonobese diabetic female mice aged 3-5 weeks were randomly divided into anti-CD20, anti-CD20 + interleukin-10, interleukin, and control groups. Mice in each group were respectively injected with anti-CD20 monoclonal antibody, anti-CD20 monoclonal antibody + adenovirus vector-mediated murine interleukin-10, adenovirus vector-mediated murine interleukin-10 and normal saline on days 1, 8, 15 and 21via tail vein. RESULTS AND CONCLUSION:At 12 weeks, the blood glucose level of mice treated with anti-CD20 monoclonal antibody and/or interleukin-10 was significantly reduced compared with the control group, while the insulin, interleukin-10 and CD20 expression levels in the serum and liver were significantly increased, the liver PDX1 expression was also upregulated. Anti-CD20 monoclonal antibody with interleukin-10 had more obvious effects than the single use. No matter the combined intervention or single use, anti-CD20 monoclonal antibody and interleukin-10 show no impact on the inflammation of liver cels. Anti-CD20 monoclonal antibody and/or interleukin-10 increases PDX1 expression in nonobese diabetic mice.