RESUMEN
Chimeric antigen receptor (CAR) serves as the foundational element of CAR-T cells. Exogenous CAR molecules can exert functional effects on allogeneic T cells, leading to their activation and subsequent functional alterations. Here we show a new method based on this biological principle: the transfer of CAR molecules from exogenous cells to the membrane of receptor T cells. This process facilitates receptor T cell to recognize target antigens and induces their activation. These patches imbued normal T cells with enhanced tumor targeting capabilities and activated their inherent killing functions. This method's efficacy introduces an approach for constructing non-genetically manipulated CAR-T cells and holds potential for application to other immune cells.
RESUMEN
Macrophages play a critical role in the body's defense against cancer by phagocytosing tumor cells, presenting antigens, and activating adaptive T cells. However, macrophages are intrinsically incapable of delivering targeted cancer immunotherapies. Engineered adoptive cell therapy introduces new targeting and antitumor capabilities by modifying macrophages to enhance the innate immune response of cells and improve clinical efficacy. In this study, we developed engineered macrophage cholesterol-AS1411-M1 (CAM1) for cellular immunotherapy. To target macrophages, cholesterol-AS1411 aptamers were anchored to the surface of M1 macrophages to produce CAM1 without genetic modification or cell damage. CAM1 induced significantly higher apoptosis/mortality than unmodified M1 macrophages in murine breast cancer cells. Anchoring AS1411 on the surface of macrophages provided a novel approach to construct engineered macrophages for tumor immunotherapy.