Objective The non-specific antitumor immunity effect of 4-1BBL-B7-H3 gene was investigated by establishing an oral squamous cell carcinoma human peripheral blood lymphocyte-severe combined immunodeficient (SCID) mice chimeric model.Methods Forty mice were randomly divided into five groups. All groups, except the non-immune reconstitution group (group D), had reconstructed human partial immune system. The control group (group A) was injected with Tca8113 cells. The Ad4-1BBL-B7-H3 group (group B) was injected with Tca8113 cells transfected by adenovirus containing 4-1BBL-B7-H3 gene. The empty vector group (group C) was injected with Tca8113 cells transfected by adenovirus containing an empty vector. The non-immune reconstitution group (group D) was injected with Tca8113 cells. The non-tumor group (group E) was injected with PBS. The tumor volumes in each group were measured weekly. Human IgG in blood was obtained through the tail vein and was determined by enzyme-linked immu-nosorbent assay. Human CD3+ and D56+ lymphocytes were assessed by flow cytometry. Model animals were killed on the ninth week. Differences in the expression of the natural killer group 2 member D (NKG2D) and toll-like receptor 2 (TLR2) in tumor tissues of each group were observed by im-munohistochemical method. 4-1BBL-B7-H3 gene expression in mice tumor tissues was detected by reverse transcription polymerase chain reaction (PCR) and the expressions of major histocompatibility complex 1 class related molecule (M1C) A, M1CB, and TLR2 were detected by real-time quantitative PCR.Results The tumor volumes of group B were remarkably lower than those in the other groups (PConclusion The high 4-1BBL-B7-H3 gene expression in tumor tissues could successfully induce the proliferation of CD3+ and CD56+ lymphocytes. This expression can also directly or indirectly activate TLR2 and up-regulate the expression of NKG2D and its ligands (M1CA and M1CB), which result in an effective antitumor immune response.
