Back

Genetic ablation of adhesion ligands averts rejection of allogeneic immune cells

Hammer, Q.; Perica, K.; van Ooijen, H.; Mbofung, R.; Momayyezi, P.; Varady, E.; Martin, K. E.; Pan, Y.; Jelcic, M.; Groff, B.; Abujarour, R.; Krokeide, S.; Lee, T.; Williams, A.; Goodridge, J. P.; Valamehr, B.; Onfelt, B.; Sadelain, M.; Malmberg, K.-J.

2023-10-09 immunology
10.1101/2023.10.09.557143 bioRxiv
Show abstract

Allogeneic cell therapies hold promise for broad clinical implementation, but face limitations due to potential rejection by the recipient immune system. Silencing of beta-2-microglobulin (B2M) expression is commonly employed to evade T cell-mediated rejection, although absence of B2M triggers missing-self responses by recipient natural killer (NK) cells. Here, we demonstrate that deletion of the adhesion ligands CD54 and CD58 on targets cells robustly dampens NK cell reactivity across all sub-populations. Genetic deletion of CD54 and CD58 in B2M-deficient allogeneic chimeric antigen receptor (CAR) T and multi-edited induced pluripotent stem cell (iPSC)-derived NK cells reduces their susceptibility to rejection by NK cells in vitro and in vivo without affecting their anti-tumor effector potential. Thus, these data suggest that genetic ablation of adhesion ligands effectively alleviates rejection of allogeneic immune cells for immunotherapy.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.