[Regulatory effect of FK506 on the expression of CD152 and PD-1 in the liver allo-recipients].

AIM

To dynamically observe the expression of CTLA-4/CD152 and PD-1 on T cell surface in the peripheral blood of liver allo-recipients, and to explore the regulatory effect of FK506 on negative costimulatory molecules.

METHODS

The blood concentration of FK506 was measured by enzyme-multiplied immunoassay technique. Flow cytometry (FCM) was used to determine the expression of T cell subsets and CD152, PD-1 on T cell surface in the peripheral blood.

RESULTS

There was no significant difference in blood concentration of FK506 between each group (P > 0.05). With the progression of treatment, the frequency of CD4(+) T cells gradually decreased and was obviously lower than that in health control until the third month (P < 005). The expression of CD4(+) T cells in each treatment group was significantly lower than that in disease control group (P < 0.05). And the frequency of CD8(+) T cells in each treatment group was obviously higher than that in disease control group (P < 0.05). After liver transplantation, the expression of CD152 on CD4(+) and CD8(+) T cells was higher than that in health control group (P < 0.05), and the expression in the second week and first month was higher than that in disease control group (P < 0.05). The frequencies of CD4(+) CD152(+) T cells in the second and third month were lower than that in the second week and first month (P < 0.05). The frequency of CD8(+) CD152(+) T cells in the third month was lower than that in the second week and first month (P < 0.05). After liver transplantation, the expression of PD-1 on T cell subsets had the tendency of advancing. Its expression on CD4(+) T cells was significantly higher than that in health control group from the second week (P < 0.05), and the expression on CD8(+) T cells increased obviously from the first month compared with that in disease control group (P < 0.05).

CONCLUSION

FK506 could up-regulate the expression of negative costimulatory molecules CD152 and PD-1 on T cell surface and inhibit the proliferation and activation of effector T cells, which may contribute to maintain the survival and homeostasis of allo-recipients.