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Fig. 1 | Renal Replacement Therapy

Fig. 1

From: Dysfunction of natural killer cells in end-stage kidney disease on hemodialysis

Fig. 1

NK cell receptor expression and function in end-stage kidney disease and chronic hemodialysis. a Uremic patients suffer from excessive inflammatory cytokine and oxidative stress concurrent with maintenance HD. Chronic exposure to oxidative stress could be responsible for downregulation of the activating receptors on NK cells. Various types of stress, including oxidative stress-induced genotoxic stress, modulate expression of ligands for NK activating receptors. Moreover, surface expression levels of membrane ligands on stressed cells can be finely tuned by the regulation of their release in soluble form by various processes including protease-mediated cleavage. b To achieve appropriate effector function, NK cells must recognize and distinguish healthy “self” cells from abnormal “non-self” cells via receptor-ligand interactions at the cell surface. Generally, the activating receptors recognize ligands on stressed cells such as tumor cells and virally infected cells, while the inhibitory receptors recognize healthy normal cells. Soluble forms of ligands can cause downregulation of surface expression of activating receptors on NK cells by promoting their internalization and degradation, leading to reduced immune responses against tumors and virally infected cells. As a result, end-stage kidney disease patients undergoing chronic dialysis are expected to be prone to tumor formation and viral expansion

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