High Expression of Tim-3 in Alveolar Echinococcosis Mediates Depletion of CD8(+)T Cell Function

Objective. CD8(+) T cells can participate in immune action by secreting various cytokines, which have a killing effect on certain viruses, tumor cells, and other antigenic substances. However, in studies such as chronic viral infections and some parasitic infections, CD8(+) T lymphocyte showed functional depletion, and its immune dysfunction was an important reason for the persistence of infection. Tim-3 has been shown to be a negative regulator of CD8(+) T cell function, causing depletion of CD8(+) T cells in cancer and chronic infection. However, the relationship between Tim-3 and CD8(+) T cells in Echinococcus multilocularis infection is not clear. Methods. In this study, we analyzed peripheral blood CD8(+) T cells from 62 alveolar echinococcosis (AE) patients and 30 healthy controls. Results. Compared with the healthy control group, the proportion of CD8(+)T cells in the peripheral blood of AE patients increased significantly, while the levels of perforin, granzyme B and IFN-gamma in peripheral blood CD8(+)T cell related factors of metabolically active alveolar echinococcosis (MAAE) patients decreased significantly. Later detection revealed that the expression of Tim-3 on CD8(+) T cells in the peripheral blood of MAAE patients was significantly higher than that of metabolically inactive alveolar echinococcosis (MIAE) patients and healthy controls. The expression levels of function-related factors perforin, granzyme B and IFN-gamma in CD8(+) Tim-3(+) T cell were significantly lower in the CD8(+) Tim-3(-) T cells of AE patients. In vitro, the secretion of CD8(+) T cell-associated factors was significantly restored by inhibiting Tim-3 expression. Conclusion. Therefore, the depletion of CD8(+)T lymphocyte in patients with alveolar echinococcosis disease is considered to be related to the high expression of Tim-3 on the surface.