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Increase in the proportion of CAR T cells expressing PD-1 post-infusion, as we observed in our transient re-expander, warrants further exploration as a biomarker that could predict response to anti-PD1 therapy after CAR T cells. CAR-negative T cells also became activated (73% HLA-DR SP + sp , up from 20% at the day 28 time-point), suggesting non-specific T-cell activation by the Pembro/Elo/Pom/Dex combination. Nonetheless, this proof-of-principle observation that CAR T-cell activity can be modulated in patients with myeloma post-infusion supports further exploration of immune-modulating therapies such as checkpoint inhibitors in combination with CAR T cells. Keywords: myeloma therapy; cellular therapies; immunotherapy; T cells EN myeloma therapy cellular therapies immunotherapy T cells 851 855 5 05/17/21 20210515 NES 210515 Autologous T cells expressing a chimeric antigen receptor (CAR) specific for B-cell maturation antigen (BCMA) have demonstrated high response rates in refractory myeloma,1-3 but relapses remain common. [Extracted from the article]

The article discusses a study on the efficacy of CD29-directed chimeric antigen receptor T-cells for sustained remissions in patients with relapsed or refractory acute lymphoblastic leukemia (ALL). Research findings presented discuss the proliferation of CTL019 cells in the blood, bone marrow and cerebrospinal fluid of patients. Data shows the survival rate among the patients and the probability of CTL019 persistence and of developing relapse-free B-cell aplasia, or cytokine-release syndrome.

The article informs that CRISPR-engineered T cells in patients with refractory cancer. It mentions that CRISPR coupled with CRISPR-associated protein 9 (Cas9) endonuclease is a powerful gene-editing technology that allows the ability to target multiple genes in T cells to improve cancer immunotherapy. It also mentions that endogenous T cell receptor and the immune checkpoint molecule programmed cell death protein 1 would improve the function and persistence of engineered T cells.