Particulate matter exposure negatively affects the cancer immunosurveillance through PD-L1 upregulation and dendritic...

The relationship between particulate matter (PM) pollution exposure and lung cancer incidence has been well established. However, the association between PM exposure and immunosurveillance, which indirectly controls tumor growth and progression, remains limited. In this study, we investigated the effect of urban particulate matter (UPM) on modulating the cancer microenvironment, particularly its impact on immunosurveillance functions. Exposure of non-small cell lung cancer (NSCLC) cell lines, A549 and NCI-H1975, to UPM induced the expression of the immune checkpoint molecule programmed cell death ligand 1 (PD-L1) in a dose-dependent manner. Additionally, UPM exposure upregulated the mRNA expression of transforming growth factor-beta (TGF-β), an immunosuppressive cytokine. The alteration in the cytokine profile upon UPM exposure impaired dendritic cell maturation, as evidenced by the retention of the CD14 monocyte marker after monocytes were exposed to UPM-treated cancer cell supernatant during the maturation process. Autologous T cells activated by UPM-treated dendritic cells exhibited reduced anti-tumor activity compared to those activated by untreated dendritic cells. This was demonstrated by the lower cancer cell death observed in cancer-T cell co-culture assays. However, there were no significant changes in immune cell populations, including CD4+ T lymphocytes, CD8+ T lymphocytes, and CD3-negative cells, between the UPM-treated dendritic cell group and the conventional dendritic cell group. This suggests that UPM affects immune function primarily in terms of quality rather than quantity. In conclusion, our findings indicate that PM exposure promotes cancer progression by altering the tumor microenvironment and impairing immunosurveillance function.