부산대학교 도서관

The immune-related adverse events resulting from the therapy of immune checkpoint inhibitors could cause kidney injury. Inflammatory reprogramming of regulatory T helper (Treg) cells or type 17 T helper (Th17) cells might be involved in the pathogenesis of nephropathy. Accumulating evidence confirms a connection between the diversity of gut microbiota and kidney diseases, suggesting that successful modification of gut microbiota could attenuate kidney injury. In other words, certain gut microbiota could contribute to the protection of kidneys via the gut-kidney axis. It has been shown that the dysbiosis of gut microbiota might affect the gut-kidney axis, leading to nephrotoxicity. On the contrary, altered levels of D-amino acids, ROS, and SCFAs through the adjustment of gut microbiota might be relevant to the reduction of nephrotoxicity. Here, we have discussed and suggested the beneficial roles of gut microbiota in the prevention of the kidney injury induced during immune-checkpoint therapy.