Effect of tumor necrosis factor-α-induced protein 8 on the immune response of CD4+ T lymphocytes in mice following acute insult.

Tumor necrosis factor-α-induced protein 8 (TNFAIP8), which was the first identified member of the TNFAIP8 family, shares considerable sequence homology with other members of the TNFAIP8 family. It is expressed in various normal human tissues, with relatively higher levels detected in lymphoid tissues and the placenta. The present study aimed to examine the effect of TNFAIP8 on cell‑mediated immunity of cluster of differentiation (CD)4+ T lymphocytes in a cecal ligation and puncture (CLP) murine model. A total of 100 male mice were randomly divided into four groups as follows: The sham injury group (n=30), the CLP group (n=30), the CLP with lentivirus‑RNA‑TNFAIP8 group (n=20) and the CLP with negative control group (n=20), and they were sacrificed 24 h following CLP. Splenic CD4+ T cells were isolated using MACS microbeads. T cell proliferation was analyzed using the MTT assay, and cytokine levels were determined with ELISA kits. Upregulation of TNFAIP8 by lentivirus‑RNA‑TNFAIP8 infection was demonstrated to promote CD4+ T lymphocyte proliferative activity following CLP, and the increase in TNFAIP8 expression in vivo affected splenic CD4+ T lymphocyte polarization following CLP‑induced sepsis. In conclusion, TNFAIP8 expression following CLP may be associated with the pathogenesis of immune dysfunction in splenic T lymphocytes in mice.