Table 1.
Exosome Source | Setting | Therapy | Tumour | Study Outcome | Reference |
---|---|---|---|---|---|
Macrophages (RAW 264.7) | In Vivo | PTX/DOX | Lung Mets | Exosomal PTX preferentially accumulated in cancer cells | [9] |
Ascites-derived | Clinical trial | AEX alone or AEX + GM-CSF | Colorectal | AEX + GM-CSF was safe, nontoxic, tolerable, and induced a beneficial tumour-specific anti-tumour CTL response | [14] |
Dendritic cells | Clinical trial | MHC Class II peptides | Melanoma | Large scale exosome production was feasible and exosome administration was safe and well tolerated | [15] |
Dendritic cells | Clinical trial | MAGE (tumour antigens) | Lung | Therapy well tolerated with some experiencing long term stable disease and activation of immune effectors | [16] |
Dendritic cells | In Vivo | IL-4 + GM-CSF | Breast | Eradication/suppression of growth of pre-established tumours in a T-cell dependant manner | [17] |
Dendritic cells | In Vivo | MHC Class I | Melanoma | MHC Class I restricted CD8+ T-cell expansion and differentiation | [18] |
Dendritic cells | In Vivo | CpG Adjuvant | Melanoma | Combination of exosomes and TLR 3 + 9 triggered efficient MHC-restricted CD8+ T-cell responses | [19] |
Dendritic cells | In Vivo | DC-Exo alone | Melanoma | DC-Exo promoted IL-15Rα- and NKG2D-dependent NK cell proliferation and activation which resulted in anti-metastatic effects | [20] |
Dendritic cells | In Vitro | DC-Exo alone | Breast | Incorporation of DC-Exo by tumour cells increased ability to activate T-cells for a more effective response | [21] |
Brain endothelial cells | In Vivo | rhodamine 123, PTX, DOX | Brain | Exosome delivery allowed DOX and PTX to cross the BBB which resulted in cytotoxicity against U-87 MG cells | [22] |
Abbreviations: AEX—Ascites-derived exosomes; GM-CSF—granulocyte-macrophage colony-stimulating factor; CTL—cytotoxic T lymphocyte; PTX—Paclitaxel; Dox—Doxorubicin; IL—Interleukin; MAGE—Melanoma-associated antigen; DC—Dendritic Cell.