fig6

Figure 6. Immunomodulatory functions of EVs. EVs derived from immune cells, MSCs, and cancer cells exhibit diverse immunomodulatory effects. Macrophage-derived EVs display polarization-dependent functions: pro-inflammatory M1-EVs activate CD4⁺ T cells, CTLs, and NK cells, whereas anti-inflammatory M2-EVs foster regulatory T cell (Treg) generation and immunosuppression. Additionally, DC-derived EVs, which express CD8, CD86, ICAM-1, and MHC I/II complexes, can transfer antigen-presenting capacity to other APCs, thereby activating CD4⁺ and CD8⁺ T cells and NK cells to enhance antitumor immunity. EVs derived from mesenchymal stem cells modulate the functions of macrophages, PBMCs, and T-cell subsets in a donor- and context-dependent manner. Conversely, tumor-derived EVs carry molecules such as DNA, PD-L1, MHC I, Hsp70, and neoantigens, which can manipulate various immune cells to drive immune evasion and tumor progression. M1 EVs: M1 macrophage-derived extracellular vesicles; M2 EVs: M2 macrophage-derived extracellular vesicles; APC: antigen-presenting cell; EVs: extracellular vesicles; MSC-EVs: mesenchymal stem cell-derived extracellular vesicles; MSCs: mesenchymal stem cells; PBMCs: peripheral blood mononuclear cells; DCs: dendritic cells; CTL: cytotoxic T lymphocyte; T_reg: regulatory T cell; NK cells: natural killer cells; DNA: deoxyribonucleic acid; PD-L1: programmed death-ligand 1; MHC I: major histocompatibility complex class I; Hsp70: heat shock protein 70.