Figure 1.

Extracellular vesicle mediated immune activation and immune suppression. (A) EVs containing MHC class from donor cells (either from tumor cells or from APCs) could bind with T cell receptor thereby inducing downstream signals to the T cell; (B) the activated T cells are further capable to release EVs loaded with TCR-β, TCR-ε, TCR-ζ that promote enhanced immune action and cytotoxicity in recipient cells; (C) EVs harboring FasL may have inherent ability to interact with corresponding Fas receptor present on T cells and induce signals down to T cell allowing the activation of downstream caspases which ultimately result into caspase induced T cell apoptosis. (C) Conversely, the caspases activity could be minimizing by EV-associated MMPs which convert membranous FasL into soluble FasL. This inhibits the interaction of FasL to Fas receptor, thus blocking the signals to caspases (17). EVs, extracellular vesicles; MHC, major histocompatibility complex; APC, antigen presenting cell; TCR, T cell receptor; FasL, Fas ligand; sFasL, soluble Fas ligand; MMPs, matrix metalloproteinases.