Role of T cells in ischemic acute kidney injury and repair

Abstract

Ischemic acute kidney injury (AKI) is a common medical problem with significant mortality and morbidity, affecting a large number of patients globally. Ischemic AKI is associated with intrarenal inflammation as well as systemic inflammation; thus, the innate and adaptive immune systems are implicated in the pathogenesis of ischemic AKI. Among various intrarenal immune cells, T cells play major roles in the injury process and in the repair mechanism affecting AKI to chronic kidney disease transition. Importantly, T cells also participate in distant organ crosstalk during AKI, which affects the overall outcomes. Therefore, targeting T cell-mediated pathways and T cell-based therapies have therapeutic promise for ischemic AKI. Here, we review the major populations of kidney T cells and their roles in ischemic AKI.

Keywords: Acute kidney injury; Inflammation; Ischemia; Reperfusion injury; T-lymphocytes.

Figure 1

Proinflammatory and anti-inflammatory T cells in ischemic acute kidney injury. T helper 1 cell (Th1), Th17, γδ T cells, and type I natural killer (NK) T cells (NKT1) promote renal injury and exert a proinflammatory effect in ischemic acute kidney injury, whereas regulatory T cells (Tregs), double-negative (DN) T cells, Th2 cells, and type II NK T cells (NKT2) play protective roles and have anti-inflammatory properties. Numbers of key landmark studies for each subset of T cells are presented. IL, interleukin; TNF-α, tumor necrosis factor α; IFN-γ, interferon γ.