https://www.selleckchem.com/pr....oducts/gilteritinib-
Effectively activating host immunity against cancer has already become a promising therapeutic strategy. However, cancer cells resist to the host immune response through both innate and adaptive immune effectors. Especially, CD47 on tumor cells protects them from macrophage phagocytosis through interaction with SIRPα, while PD-L1 interacts with its receptor PD-1 and dampens T cell-mediated tumor killing. Herein, we report that genetically programmable fusion cellular vesicles (Fus-CVs) displaying high-affinity SIRPα variant
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