UCARTMESO

TRAC KO limits the risk of GvHD, while CD52 KO allows the use of alemtuzumab in the preconditioning regimen. The data shows that cells not edited at the TGFBR2 locus are unable to be activated upon target exposure in the presence of TGFβ, while edited cells were activated in the presence of TGFβ, triggering CD25 expression at similar levels as those of cells activated in the absence of TGFβ. Conclusions Altogether, we have demonstrated potent antitumor activity in vitro and in vivo, and that addition of the third knock-out of TGFBR2 gene provide valuable additional properties to UCARTMeso cells, representing a very attractive strategy for their use in the treatment of solid tumors.