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The protumorigenic effects of inflammation have been well studied; however, less is known about the effect of inflammation on resistance to immunotherapy. The authors here demonstrated that targeting the COX2/PGE2/EP2-4 axis with nonsteroidal and steroidal anti-inflammatory drugs reshapes the immune microenvironment toward an antitumor inflammatory state, and in combination with immune checkpoint blockade increased the intratumoral accumulation of T cells with improved effector function.
These findings identify a mechanism by which anti-inflammatory drugs alter the tumor immune microenvironment and suggest that combining anti-inflammatory drugs with immune checkpoint blockade is a promising avenue to increase the efficacy of immunotherapy in patients.
The protumorigenic effects of inflammation have been well studied; however, less is known about the effect of inflammation on resistance to immunotherapy. The authors here demonstrated that targeting the COX2/PGE2/EP2-4 axis with nonsteroidal and steroidal anti-inflammatory drugs reshapes the immune microenvironment toward an antitumor inflammatory state, and in combination with immune checkpoint blockade increased the intratumoral accumulation of T cells with improved effector function.
These findings identify a mechanism by which anti-inflammatory drugs alter the tumor immune microenvironment and suggest that combining anti-inflammatory drugs with immune checkpoint blockade is a promising avenue to increase the efficacy of immunotherapy in patients.
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This work was supported by Cancer Research UK Institute Award (A19258; to V.S. Pelly, A. Moeini, E. Bonavita, C. Hutton, A. Blanco-Gomez, A. Banyard, C.R. Bell, E. Flanagan, S-C. Chiang, C. Jørgensen, and S. Zelenay), a research agreement with Ono Pharmaceutical (to A. Moeini and S. Zelenay), and an ERC CoG Disect (772577; to C. Jørgensen).