Fig. 3.

A summary of tumor cell killing mechanisms by CAR cells originating from different cell types. In conventional CAR T therapy, tumor cell apoptosis is primarily triggered by CAR recognition of tumor-associated antigens (TAA) and the release of granzymes, perforins, and other cytokines. Since this therapy is prone to side effects like GVHD, other cell types such as NK cells and certain T cell subtypes are being investigated. These cell types exert tumor-killing effects independent of the αβTCR, mainly through receptors like Fas, NKR, and CD16. Moreover, macrophages compensate for the ineffectiveness of other cells in targeting solid tumors. In addition to CAR-based recognition, CAR-Macrophages can reeducate the M2 subtype of macrophage into the M1 subtype, releasing proinflammatory cytokines to trigger further immune response against the tumor.