Table 2.
Study | EV Concentration | Cellular Origin of EV | EV Pathological Significance | Reference |
---|---|---|---|---|
Burbano, C.; et al. | Increased in SLE compared to healthy controls | platelet | Formation of immune complexes, source of nuclear antigens, correlation with disease activity |
[52] |
López, P.; et al. | Increased in SLE compared to healthy controls | platelet, monocyte, T lymphocyte |
EV level correlated with: disease activity, glucocorticoid therapy, endothelial vasodilatation |
[58] |
Atehortúa, L.; et al. | Endothelial cell activation, endothelial injury, |
[60] | ||
Winberg, L.-K.; et al., Dieker, J.J.; et al., Rother, N.; et al. |
In vitro stimulation of polymorphonuclear leukocytes with EV from SLE patients increased ROS production EV promote neutrophil activation and NETs production |
[63,64,65] | ||
Nielsen, C.T.; et al., Rasmussen, N.S.; et al. |
IgG/galectin-3 binding protein (G3BP)+ EV are involved in the pathogenesis of lupus nephritis | [67,68] | ||
Lu, J.; et al., Vanegas-García, A.; et al. |
Urinary podocyte-derived EV increased in SLE | Urinary EV | Urinary podocyte-derived EV level correlated with systemic disease activity and renal injury Urinary EV high-mobility group box 1 molecule (HMGB1)+ were found to be higher in lupus nephritis |
[69,70] |
Felip, M.L.; et al., Solé, C.; et al., Navarro-Quiroz, E.; et al., Li, Y.; et al., Garcia-Vives, E.; et al. |
EV derived miRNA | miR-21, miR-150, and miR-29c, miR-31, miR-107, and miR-135b-5p correlated with renal injury in lupus nephritis | [72,73,74,75,76] | |
Mobarrez, F.; et al. | EV containing mitochondrial molecules (mitoEV) | mitoEV were associated with disease activity, immune complex formation and renal damage | [77] |