T-cells can recognize and kill tumour cells by using similar mechanisms as for eradicating virally infected cells. T-cells kill their targets through induction of apoptosis, either via death receptors or by secretion of granzymes and perforin.
Chimeric antigen receptors (CARs) are human leukocyte antigen (HLA)-independent fusion molecules that couple the binding of a native tumour-associated target, displayed on the surface of tumour cells, to the delivery of a tailored T-cell activating signal. T-cells genetically engineered to express CAR receptors efficiently recognize and kill their target cells. Since an antibody scFv is used to retarget the T-cell, they can be targeted to any available cell surface marker on the tumour cell[1,2].
CAR T-cells can be easily engineered from patient blood and reinfused to the patient after ex vivo expansion. Most of the CARs in current clinical trials join an extracellular single-chain variable fragment (scFv) with the T cell receptor CD3ζ signaling domain as well as an additional domain, CD28 or 4-1BB, to supply a co-stimulatory signal, which appears to be vital for in vivo expansion and persistence.
 Karlsson, H. (2016). "Approaches to augment CAR T-cell therapy by targeting the apoptotic machinery." Biochem Soc Trans 44(2): 371-376.
 Whilding, L. M., et al. (2016). "The integrin alphavbeta6: a novel target for CAR T-cell immunotherapy?" Biochem Soc Trans 44(2): 349-355.
 Singh, N., et al. (2016). "CAR T Cell Therapy in Acute Lymphoblastic Leukemia and Potential for Chronic Lymphocytic Leukemia." Curr Treat Options Oncol 17(6): 28.