Clinical significance of CCR7(+)CD8(+) T cells in kidney transplant recipients with allograft rejection

The regulatory function of CCR7(+)CD8(+) T cells against effector T-cells involved in T-cell mediated rejection (TCMR) in kidney transplant recipients was investigated. In vitro experiments explored the ability of CCR7(+)CD8(+) T cells to suppress T-cell proliferation under T-cell activation conditions or during coculture with human renal proximal tubular epithelial cells (HRPTEpiC). In an ex vivo experiment, the proportion of CCR7(+)/CD8(+), FOXP3(+)/CCR7(+)CD8(+) T and effector T-cell subsets were compared between the normal biopsy control (NC, n = 17) and TCMR group (n = 17). The CCR7(+)CD8(+) T cells significantly suppressed the proliferation of CD4(+) T cells and significantly decreased the proportion of IFN-γ(+) and IL-17(+)/CD4(+) T cells and inflammatory cytokine levels (all p < 0.05). After coculturing with HRPTEpiC, CCR7(+)CD8(+) T cells also suppressed T-cell differentiation into IL-2(+), IFN-γ(+), and IL-17(+)/CD4(+) T cells (all p < 0.05). The TCMR group had significantly fewer CCR7(+)/CD8(+) and FOXP3(+)/CCR7(+)CD8(+) T in comparison with the NC group, but the proportions of all three effector T-cell subsets were increased in the TCMR group (all p < 0.05). The proportion of CCR7(+)/CD8(+) T was inversely correlated with those of effector T-cell subsets. The results indicate that CCR7(+)CD8(+) T cells may regulate effector T-cells involved in TCMR in an in vitro and in an ex vivo transplant model.