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Vaccine-boosted CAR T crosstalk with host immunity to reject tumors with antigen heterogeneity. | LitMetric

Vaccine-boosted CAR T crosstalk with host immunity to reject tumors with antigen heterogeneity.

Cell

David H. Koch Institute for Integrative Cancer Research, MIT, Cambridge, MA 02139, USA; Department of Materials Science and Engineering, MIT, Cambridge, MA 02139, USA; Department of Biological Engineering, MIT, Cambridge, MA 02139, USA; Ragon Institute of Massachusetts General Hospital, Cambridge, MA 02139, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Electronic address:

Published: July 2023

AI Article Synopsis

Article Abstract

Chimeric antigen receptor (CAR) T cell therapy effectively treats human cancer, but the loss of the antigen recognized by the CAR poses a major obstacle. We found that in vivo vaccine boosting of CAR T cells triggers the engagement of the endogenous immune system to circumvent antigen-negative tumor escape. Vaccine-boosted CAR T promoted dendritic cell (DC) recruitment to tumors, increased tumor antigen uptake by DCs, and elicited the priming of endogenous anti-tumor T cells. This process was accompanied by shifts in CAR T metabolism toward oxidative phosphorylation (OXPHOS) and was critically dependent on CAR-T-derived IFN-γ. Antigen spreading (AS) induced by vaccine-boosted CAR T enabled a proportion of complete responses even when the initial tumor was 50% CAR antigen negative, and heterogeneous tumor control was further enhanced by the genetic amplification of CAR T IFN-γ expression. Thus, CAR-T-cell-derived IFN-γ plays a critical role in promoting AS, and vaccine boosting provides a clinically translatable strategy to drive such responses against solid tumors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10372881PMC
http://dx.doi.org/10.1016/j.cell.2023.06.002DOI Listing

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