Extracellular vesicles as mediators of vascular inflammation in kidney disease

Figure 2 Roles of extracellular vesicles in leukocyte function in the atherosclerotic plaque. Data on interaction of EVs with neutrophilic granulocytes, monocytes and mononuclear phagocytes and T lymphocytes is summarized. Regarding neutrophilic granuloctes (PMN), platelet EVs (P-EV) promote neutrophil (PMN) adhesion to the endothelium, neutrophil EVs (N-EV) mostly decrease adhesion and migration through the endothelium. Regarding monocytic cells, endothelial (En-EV) and P-EVs promote adhesion to the endothelium. Inside the plaque, En-EVs promote antigen presenting cell (APC) maturation and cytokine production and erythrocyte EVs (Er-EVs), monocyte EVs (M-EVs) and T cell EVs (T-EVs) increase cytokine production. T-EVs also increase lipid uptake. N-EVs suppress activation. Regarding T cells, P-EVs decrease cytokine production, En-EVs promote T cell proliferation and TH1 differentiation. EVs: Extracellular vesicles.