potential immune modulatory action of mesenchymal stem cell derived extracellular vesicles in type 1 diabetes

Several preclinical studies have shown potential immunemodulatory properties of mesenchymal stem cells (MSC) in type 1 diabetes leading to phase I/II clinical trials. Immune-modulatory properties of MSC have been mainly ascribed to their secretome. The extracellular vesicles (EV) have emerged as paracrine mediators of MSC actions. In fact, MSC-derived EV have been shown to carry proteins and nucleic acids capable to mimic the effect of originating cells. In the present short review we discuss evidences for contribution of EV to the immune-modulatory properties of MSC and mechanisms involved. In particular, EV were shown to inhibit T cell response to the glutamic acid decarboxylase (GAD) islet auto-antigen by inducing a shift of lymphocytes from Th1 to Th2 phenotype

Extracellular vesicle-mediated modulation of angiogenesis

Angiogenesis is a tightly regulated process where a number of different players are involved. Recently, a role for membrane vesicles actively released from cells has been proposed. Virtually all cell types may release non-apoptotic membrane vesicles in the nano-size range containing critical components of the cell of origin. The two main categories of these vesicles include exosomes and microvesicles that differ for biogenesis but, sharing several features and mechanisms of action, have been collectively named extracellular vesicles (EV). EV are able to transfer from one cell to another bioactive lipids, proteins and nucleic acids that may induce changes in the phenotype and functions of the recipient cells. This new mechanism of cell to cell communication has been involved in modulation of the angiogenic process. Tumor cells, inflammatory cells and stem/progenitor cells were shown to release EV with angiogenic properties, suggesting that they may act on vascular remodeling in different physiological and pathological conditions. In this review we discuss the evidence for the role and the mechanisms of action of EV in vascular homeostasis and in the angiogenic processes occurring in tumors, inflammation and tissue regeneration