Dual role of T cell subsets in renal injury

T cells and their subsets play dual roles in the pathogenesis, progression, and repair of kidney injury, acting as both drivers of inflammation and fibrosis and regulators of immune homeostasis and tissue repair. Although previous research has predominantly focused on the role of T cells in classic immune-mediated kidney diseases such as lupus nephritis and glomerulonephritis, with relatively less emphasis on their involvement in broader kidney injury contexts, emerging evidence reveals a more extensive and spatiotemporally specific regulatory network of T-cell subsets in acute kidney injury (AKI), chronic kidney disease (CKD), and transplant kidney injury. Within the pathological processes of kidney injury, distinct T-cell subsets contribute to disease progression through specific mechanisms. For instance, Th17 cells exacerbate acute and chronic inflammation and fibrosis via IL-17-dependent pathways, yet may contribute to repair in later injury phases. This review primarily outlines the impact of different T-cell subsets on kidney injury and explores strategies for their therapeutic targeting.