Abstract
Immune inflammation is crucial in mediating acute kidney injury (AKI). Immune cells of both the innate and adaptive immune systems substantially contribute to overall renal damage in AKI. Regulatory T cells (Tregs) are key regulator of immunological function and have been demonstrated to ameliorate injury in several murine experimental models of renal inflammation. Recent studies have illuminated the renal-protective function of Tregs in AKI. Tregs appear to exert beneficial effects in both the acute injury phase and the recovery phase of AKI. Additionally, Tregs-based immunotherapy may represent a promising approach to ameliorate AKI and promote recovery from AKI. This review will highlight the recent insights into the role of Tregs and their therapeutic potential in AKI.
Highlights
Acute kidney injury (AKI) is caused by multiple etiologies that lead to renal dysfunction within a short period of time
Tregs maintain close interaction with immature dendritic cells (DCs) through lymphocyte activation gene-3 (Lag-3)/MHC II molecules [30], leukocyte function-associated antigen-1 (LFA-1)/intercellular adhesion molecule 1 (ICAM-1) [31], and neuropilin-1 (Nrp1) [32] on their cell surface and rely on CTLA-4 to inhibit the maturation of DCs [33]
Ischemic preconditioning (IPC) is partially mediated by Tregs and significantly inhibits the accumulation of neutrophils and macrophages, tubular necrosis, and loss of kidney function caused by a subsequent renal Ischaemia reperfusion injury (IRI) one week later [47]
Summary
Acute kidney injury (AKI) is caused by multiple etiologies that lead to renal dysfunction within a short period of time. Previous studies have revealed that immune inflammation is crucial in mediating AKI [5]. Immune cells of both the innate and adaptive immune systems, including dendritic cells (DCs), natural killer T cells, T and B lymphocytes, neutrophils, and macrophages, are well known for their participation in early injury [6]. Control of kidney inflammation can significantly reduce kidney damage in AKI [7, 8]. Removing, inhibiting, or antagonizing neutrophils, macrophages, T cells, and B lymphocytes have been shown to suppress renal inflammation and protect in vivo AKI models to varying degrees [9]. We examine the research progress of Tregs in AKI
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