Abstract
Dexamethasone (dex) is a glucocorticoid that is a mainstay for the treatment of inflammatory pathologies, including immunotherapy-associated toxicities, yet the specific impact of dex on the activity of CAR Tcells is not fully understood. We assessed whether dex treatment given exvivo or as an adjuvant invivo with CAR Tcells impacted the phenotype or function of CAR Tcells. We demonstrated that CAR Tcell expansion and function were not inhibited by dex. We confirmed this observation using multiple CAR constructs and tumor models, suggesting that this is a general phenomenon. Moreover, we determined that dex upregulated interleukin-7 receptor α on CAR Tcells and increased the expression of genes involved in activation, migration, and persistence when supplemented exvivo. Direct delivery of dex and IL-7 into tumor-bearing mice resulted in increased persistence of adoptively transferred CAR Tcells and complete tumor regression. Overall, our studies provide insight into the use of dex to enhance CAR Tcell therapy and represent potential novel strategies for augmenting CAR Tcell function during production as well as following infusion into patients.
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