Figure 1.

The roles of diverse lymphocyte subsets on AKI and renal fibrosis. Different subsets of T cells, innate-like lymphocytes, and innate lymphoid cells mediate renal injury and fibrosis by regulating intrinsic cell death, proliferation, and fibroblast formation. In the process, cytokine secretion and cytotoxicity are two major mechanisms. Some subsets of lymphocytes, such as Th1, Th17, type I NKT cells, and γδT cells, produce pathogenic cytokines like IFN-γ, induce renal inflammatory, and impair TECs and VECs, resulting in the decline of renal function and exacerbation of renal fibrosis. While MAIT cells play the pathogenic role by cytotoxicity. Other subtypes, such as Tregs, DNT cells, ILC2, and type II NKT cells, produce protective cytokines like IL-10, reduce renal inflammation, promote TEC repair, leading to preserve renal function and alleviate renal fibrosis. In addition, Th2 and CD8⁺ T cells have dual roles in AKI and CKD. Cells colored red represent that they are pathogenic. Cells colored blue represent that they are protective. Cells colored orange represent that they have dual roles. The rectangle with red background represents the pathogenic role and that colored blue means the protective role. The up arrows mean increased roles, and the down arrows mean decreased roles. Th, T helper cell; NKT, natural killer cell; γδT, γδ⁺T cell; MAIT, mucosa-associated invariant T cell; Treg, regulatory T cell; DNT, double-negative T cell; ILC2, type 2 innate lymphoid cell; MAIT, mucosa-associated invariant T cell; IFN-γ, interferon γ; IL, interleukin; TEC, tubular epithelial cell; VEC, vascular endothelial cell.