T lymphocytes and acute kidney injury: update

Abstract

The immune system is among the key pathogenic factors in acute kidney injury (AKI). Various immune cells, including dendritic cells, natural killer T cells, T and B lymphocytes, neutrophils and macrophages are involved. Conventional CD4+ lymphocytes are well established to participate in early injury, and CD4+CD25+FoxP3 regulatory T cells are protective and can accelerate repair. A newly identified kidney T cell receptor + CD4-CD8- (double-negative) T cell has complex functions, including potentially anti-inflammatory roles in AKI. In this mini review, we summarize the data on the role of lymphocytes in AKI and set the stage for further mechanistic studies as well as interventions to improve outcomes.

Fig. 1

Immune cells in AKI – overview and introduction of the DN T cell. Immune cells reside in the kidney steady state and increase after IRI. T cells contribute to increased vascular permeability after IRI and important roles are played in AKI by dendritic cells (DCs), macrophages, NK and NKT cells, B cells and neutrophils. During the reperfusion phase, these cells adhere to activated endothelium and other cells responding to cytokines, chemokines, oxygen free radicals, complement, coagulant factors, and other mediators. This triggers the inflammatory cascade and increases cytokine levels (IFN-γ and TNF-α, for example) that mediate inflammation after ischemia. TLRs = Toll-like receptors. Panels represent the outer medulla (modified with permission [1]).