Comparison of the immunomodulatory potential of platinum-based anti-cancer drugs and anthracyclins on human monocyte-derived cells.
Viktória JeneiSára BuraiTamás MolnárBalázs KardosRebeka MácsikMárta TóthZsuzsanna DebreceniAttila BácsiAnett MázlóGábor KonczPublished in: Cancer chemotherapy and pharmacology (2022)
Macrophages and dendritic cells (DCs) are important contributors to anti-tumor immune responses. However, these highly plastic cells are also the primary targets of tumor manipulation, which may result in the development of tumor-promoting subtypes. The effect of chemotherapeutic agents on tumor cells is an area of intense study, but little is known about their effects on innate immune cells.We investigated the effects of four chemotherapeutic drugs (two platinum-based agents; oxaliplatin and cisplatin, and two anthracyclines; doxorubicin and epirubicin) on the differentiation, function, and viability of macrophages and DCs. Macrophages and DCs were differentiated from monocytes in the presence of these chemotherapeutic drugs and we compared their cell surface receptor expression, cytokine production, and chemotactic- and T-cell-polarizing ability.We have shown that differentiation in the presence of anthracyclines dose-dependently increases CTLA-4 expression in DCs. Antineoplastic agent-driven differentiation strongly modified the CCL2- or CCL5-induced chemotactic activity of both macrophages and DCs. DCs differentiated in the presence of high-dose cisplatin and a low dose of epirubicin promoted regulatory T-cell development, whereas oxaliplatin at specific doses induced both DCs and macrophages to enhance cytotoxic T-cell responses. Furthermore, we found that inflammatory macrophages are more sensitive to doxorubicin-induced cell death than their counterparts.In summary, our results confirm that chemotherapeutic agents acting on a similar basis may have different effects on the anti-tumor immune response. Treatment with optimal dose, combinations, and timing of chemotherapy may determine tumor immunity and the metastatic potential of tumors.
Keyphrases
- immune response
- dendritic cells
- low dose
- high dose
- drug induced
- high glucose
- cell death
- liver injury
- cell cycle arrest
- induced apoptosis
- diabetic rats
- endothelial cells
- oxidative stress
- drug delivery
- squamous cell carcinoma
- cell surface
- small cell lung cancer
- regulatory t cells
- transcription factor
- cancer therapy
- mass spectrometry
- toll like receptor
- radiation therapy
- long non coding rna
- risk assessment
- inflammatory response
- human health
- endoplasmic reticulum stress
- rectal cancer
- locally advanced