Abstract
The status of cellular immunity has been shown to be associated with the occurrence and development of sepsis. Accumulating evidence has demonstrated that tumor necrosis factor-α-induced protein 8 like-2 (TIPE2) plays an important role in maintaining homeostasis of immune function. The present study, with the use of a controlled in vivo approach, demonstrated the effect of TIPE2 on cell-mediated immunity of CD4+ T lymphocytes in thermal injury murine model. One hundred and twenty-eight male mice were randomly allocated into four groups, which were sham burn group (n=48), burn group (n=48), burn with lentivirus-RNAi-TIPE2 transfection group (n=16), burn with negative control transfection group (n=16), and they were sacrificed at the designated time points. CD4+ T lymphocytes were isolated from the spleen using MACS microbeads. Phenotypes were analyzed by flow cytometry analysis, and cytokines were determined using ELISA kits. We found that the expression of TIPE2 was markedly increased in CD4+T lymphocytes in mice at 24,48 and 72 hours postburn. Down-regulation of TIPE2 by lentivirus-RNAi-TIPE2 attenuated the suppressive effect of CD4+T lymphocytes, which was associated with profound elevation of nuclear factor of activated T cell (NF-AT) activity. These results demonstrate that TIPE2 appear to be involved in the immune regulation of CD4+ T lymphocytes, and the decrease in TIPE2 expression on CD4+T lymphocytes in vivo can enhance peripheral T lymphocyte function after thermal injury. These data might provide a valid strategy to prevent the development of immunosuppressive state resulted from major burns.