A comprehensive summary of studies on targetting the MDSC-IL-10 pathway
| Study | Model | Cancer type | Strategy to suppress MDSC function |
|---|---|---|---|
| Rossowska et al. [102] | Murine | CRC | Concomitant anti-IL-10 treatment enhanced efficacy of cyclophosphamide and bone marrow-derived dendritic cell transfer therapy via limiting MDSC suppressive functions allowing enhanced NK cell anti-tumour effector function. |
| Rossowska et al. [115] | Murine | CRC | Silencing of IL-10 expression through inoculation of tumours with shRNA-IL-10 lentivectors inhibited MDSCs and suppressed cancer growth via enhanced anti-tumour type 1 immune response. |
| Gupta et al. [116] | Murine | Breast cancer (triple negative) | Oral atovaquone treatment reduced tumour MDSCs and IL-10 in HCC1806, CI66 and 4T1 paclitaxel-resistant (4T1-PR) breast cancer, leading to a reduction in tumour growth by 45%, 70% and 42% respectively. |
| Hu et al. [117] | Murine | HCC | HCC tumour MSDC-derived IL-10 suppressed the ability of dendritic cells to produce IL-12 and stimulate T cells. |
| Shen et al. [118] | Murine | Pancreatic cancer | IL-10 protein trap treatment reduced immunosuppressive cell function including MDSCs, leading to activation of anti-tumour cells such as NK cells thereby suppressing tumour growth. |
| Li et al. [104] | Human | Gastric cancer | Human gastric cancer patient-derived tumour MDSCs suppressed CD4+ T cells ex vivo via IL-10 in response to VIP, leading to reduced IL-2 and IFNγ production and impaired anti-tumour immunity. Inhibiting VIP may represent a viable strategy in targeting the MDSC-IL-10 pathway. |
| Gneo et al. [103] | Human | CRC | Blockade of M-MDSC-derived IL-10, but not Arg1 or iNOS, released human CRC tumour M-MDSC-mediated suppression on T cells and restored T cell proliferation. |
| Sato et al. [119] | Human | Lymphoma (non-Hodgkin’s) | Human lymphoma patients with higher IL-10 producing MDSCs (but not Arg1 or iNOS) are associated with reduced anti-tumoural NK cells in blood. |
shRNA: short hairpin RNA
