Regulation of Dendritic Cell Immune Function and Maturation by the Recombinant Antigen p53 of Trichinella spiralis

The excretion and secretion of antigens (ES) of Trichinella spiralis ( T. spiralis ) affect the maturation of dendritic cells (DCs). To assess the regulation of T. spiralis recombinant antigen p53 in the immune function and maturation of DCs, we determined the activity of DCs and the expression of indoleamine 2,3-dioxygenase (IDO). The levels of interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α) mRNA, the tryptophan concentration of the cell supernatant, DC morphology, and the levels of the surface molecules MHC-II, CD80, and CD86 in DCs were determined. We found that relative to that in the blank group, in the ES group and p53 group, the expression of IDO increased significantly, the concentration of tryptophan decreased, and the transcription levels of IL-10, IL-6, and TNF-α increased significantly. However, the IL-10 mRNA transcription level in the 1-MT (IDO inhibitor) + p53 group was considerably lower than that in the p53 group, whereas the IL-6 and TNF-α mRNA levels were substantially greater. Additionally, in the LPS group, the DC surface was wrinkled, with many burr-like protrusions and complete functional morphology. In the ES antigen group and p53 group, the number of cell surface wrinkles increased, but the number of burr-like protrusions on the surface was very small, which indicated that the ES antigen and p53 antigen inhibited the maturation of DCs. The levels of MHC-II, CD80, and CD86 in the LPS group increased relative to those in the blank group. Additionally, MHC-II expression in the p53 group was not significantly different from that in the blank group, but the CD80 and CD86 levels increased. Compared to that in the LPS group, the increase was significantly inhibited, which indicated that the p53 antigen inhibited the complete maturation of DCs. Our results laid a foundation for determining the pathogenic mechanism of T. spiralis and understanding its immune tolerance and mechanism underlying immune regulation.