Fig. 3
From: Eosinophils in the tumor microenvironment: implications for cancer immunotherapy
Eosinophils take part in a successful cancer immunotherapy. Treatment with immune checkpoint blockade (ICB) therapy and cisplatin (CIS) increases IL-5 and IL-33, which increase eosinophil differentiation and recruitment, respectively (a). Dipeptidyl peptidase-4 inhibitor (DPP4i), such as sitagliptin, actively stimulates eosinophils when combined with ICB (b). Anti-CTLA-4 alone is also capable of activating cellular immunity with CD4 + and CD8 + T cells and galvanizing eosinophils to eliminate tumor cells in synergy with T cells (c). In vitro differentiation of eosinophils from human embryonic stem cells (hESCs) could be vital strategy to create a product of eosinophils for immunotherapy. Both stem cell-differentiated eosinophils and chimeric antigen receptor (CAR) T cells can suppress tumor growth, but when combined, they synergize their tumor-killing potential (d). ICB anti-PD-1 plus anti-CTLA-4