Deletion of CD38 enhances CD19 chimeric antigen receptor T cell function.

ABSTRACT: Cell surface molecules transiently upregulated on activated T cells can play a counter-regulatory role by inhibiting T cell function. Deletion or blockade of such immune checkpoint receptors has been investigated to improve the function of engineered immune effector cells. CD38 is upregulated on activated T cells, and although there have been studies showing that CD38 can play an inhibitory role in T cells, how it does so has not fully been elucidated. In comparison with molecules such as PD1, CTLA4, LAG3, and TIM3, we found that CD38 displays more sustained and intense expression following acute activation. After deleting CD38 from human chimeric antigen receptor (CAR) T cells, we showed relative resistance to exhaustion in vitro and improved anti-tumor function in vivo. CD3

SUBMITTER: Veliz K 

PROVIDER: S-EPMC11193011 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature