CXCR2 inhibition in G-MDSCs enhances CD47 blockade for melanoma tumor cell clearance

The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust depletion of tumor-associated macrophages (TAMs). While CSF1R blockade effectively eliminates TAMs from the solid tumor microenvironment, its clinica...

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Published in:	Proceedings of the National Academy of Sciences - PNAS Vol. 121; no. 5; p. e2318534121
Main Authors:	Banuelos, Allison, Zhang, Allison, Berouti, Hala, Baez, Michelle, Yılmaz, Leyla, Georgeos, Nardin, Marjon, Kristopher D, Miyanishi, Masanori, Weissman, Irving L
Format:	Journal Article
Language:	English
Published:	United States National Academy of Sciences 30-01-2024
Subjects:	Animals Anticancer properties Biological Sciences Bone marrow Cancer immunotherapy CD47 Antigen Colony-stimulating factor CXCR2 protein Effectiveness Granulocytes Immunosuppression Immunotherapy Macrophage colony-stimulating factor Macrophages Melanoma Melanoma, Experimental Myeloid-Derived Suppressor Cells Phagocytosis Solid tumors Suppressor cells Synergism Tumor Microenvironment Tumors macrophages tumor immunology CD47 blockade myeloid-derived suppressor cells CXCR2
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Abstract	The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust depletion of tumor-associated macrophages (TAMs). While CSF1R blockade effectively eliminates TAMs from the solid tumor microenvironment, its clinical efficacy is limited. Here, we use an inducible CSF1R knockout model to investigate the persistence of tumor progression in the absence of TAMs. We find increased frequencies of granulocytic myeloid-derived suppressor cells (G-MDSCs) in the bone marrow, throughout circulation, and in the tumor following CSF1R deletion and loss of TAMs. We find that G-MDSCs are capable of suppressing macrophage phagocytosis, and the elimination of G-MDSCs through CXCR2 inhibition increases macrophage capacity for tumor cell clearance. Further, we find that combination therapy of CXCR2 inhibition and CD47 blockade synergize to elicit a significant anti-tumor response. These findings reveal G-MDSCs as key drivers of tumor immunosuppression and demonstrate their inhibition as a potent strategy to increase macrophage phagocytosis and enhance the anti-tumor efficacy of CD47 blockade in B16-F10 melanoma.
AbstractList	The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust depletion of tumor-associated macrophages (TAMs). While CSF1R blockade effectively eliminates TAMs from the solid tumor microenvironment, its clinical efficacy is limited. Here, we use an inducible CSF1R knockout model to investigate the persistence of tumor progression in the absence of TAMs. We find increased frequencies of granulocytic myeloid-derived suppressor cells (G-MDSCs) in the bone marrow, throughout circulation, and in the tumor following CSF1R deletion and loss of TAMs. We find that G-MDSCs are capable of suppressing macrophage phagocytosis, and the elimination of G-MDSCs through CXCR2 inhibition increases macrophage capacity for tumor cell clearance. Further, we find that combination therapy of CXCR2 inhibition and CD47 blockade synergize to elicit a significant anti-tumor response. These findings reveal G-MDSCs as key drivers of tumor immunosuppression and demonstrate their inhibition as a potent strategy to increase macrophage phagocytosis and enhance the anti-tumor efficacy of CD47 blockade in B16-F10 melanoma.The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust depletion of tumor-associated macrophages (TAMs). While CSF1R blockade effectively eliminates TAMs from the solid tumor microenvironment, its clinical efficacy is limited. Here, we use an inducible CSF1R knockout model to investigate the persistence of tumor progression in the absence of TAMs. We find increased frequencies of granulocytic myeloid-derived suppressor cells (G-MDSCs) in the bone marrow, throughout circulation, and in the tumor following CSF1R deletion and loss of TAMs. We find that G-MDSCs are capable of suppressing macrophage phagocytosis, and the elimination of G-MDSCs through CXCR2 inhibition increases macrophage capacity for tumor cell clearance. Further, we find that combination therapy of CXCR2 inhibition and CD47 blockade synergize to elicit a significant anti-tumor response. These findings reveal G-MDSCs as key drivers of tumor immunosuppression and demonstrate their inhibition as a potent strategy to increase macrophage phagocytosis and enhance the anti-tumor efficacy of CD47 blockade in B16-F10 melanoma. The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust depletion of tumor-associated macrophages (TAMs). While CSF1R blockade effectively eliminates TAMs from the solid tumor microenvironment, its clinical efficacy is limited. Here, we use an inducible CSF1R knockout model to investigate the persistence of tumor progression in the absence of TAMs. We find increased frequencies of granulocytic myeloid-derived suppressor cells (G-MDSCs) in the bone marrow, throughout circulation, and in the tumor following CSF1R deletion and loss of TAMs. We find that G-MDSCs are capable of suppressing macrophage phagocytosis, and the elimination of G-MDSCs through CXCR2 inhibition increases macrophage capacity for tumor cell clearance. Further, we find that combination therapy of CXCR2 inhibition and CD47 blockade synergize to elicit a significant anti-tumor response. These findings reveal G-MDSCs as key drivers of tumor immunosuppression and demonstrate their inhibition as a potent strategy to increase macrophage phagocytosis and enhance the anti-tumor efficacy of CD47 blockade in B16-F10 melanoma. This study demonstrates the efficacy of combining macrophage-checkpoint inhibition with granulocytic myeloid-derived suppressor cell (G-MDSC) targeting as a strategy for cancer immunotherapy. While CD47 blockade or CXCR2 inhibition alone were not significantly effective in combating tumor progression as single-agent therapies, their combination resulted in an enhanced anti-tumor effect. Through the inhibition of G-MDSCs immunosuppressive contributions to microenvironment, this dual-treatment strategy boosts macrophages immune response against cancer cells and delays tumor progression. We believe that these findings present a promising therapeutic approach for treating a wide range of solid tumors in which both tumor-associated macrophages and G-MDSCs are present. The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust depletion of tumor-associated macrophages (TAMs). While CSF1R blockade effectively eliminates TAMs from the solid tumor microenvironment, its clinical efficacy is limited. Here, we use an inducible CSF1R knockout model to investigate the persistence of tumor progression in the absence of TAMs. We find increased frequencies of granulocytic myeloid-derived suppressor cells (G-MDSCs) in the bone marrow, throughout circulation, and in the tumor following CSF1R deletion and loss of TAMs. We find that G-MDSCs are capable of suppressing macrophage phagocytosis, and the elimination of G-MDSCs through CXCR2 inhibition increases macrophage capacity for tumor cell clearance. Further, we find that combination therapy of CXCR2 inhibition and CD47 blockade synergize to elicit a significant anti-tumor response. These findings reveal G-MDSCs as key drivers of tumor immunosuppression and demonstrate their inhibition as a potent strategy to increase macrophage phagocytosis and enhance the anti-tumor efficacy of CD47 blockade in B16-F10 melanoma.
Author	Yılmaz, Leyla Georgeos, Nardin Marjon, Kristopher D Miyanishi, Masanori Banuelos, Allison Berouti, Hala Weissman, Irving L Zhang, Allison Baez, Michelle
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Copyright	Copyright National Academy of Sciences Jan 30, 2024 Copyright © 2024 the Author(s). Published by PNAS. 2024
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Keywords	macrophages tumor immunology CD47 blockade myeloid-derived suppressor cells CXCR2
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 1A.B. and A.Z. contributed equally to this work. Contributed by Irving L. Weissman; received October 24, 2023; accepted December 16, 2023; reviewed by Alberto Mantovani, Dmitry Gabrilovich, and Justin D. Lathia
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Snippet	The use of colony-stimulating factor-1 receptor (CSF1R) inhibitors has been widely explored as a strategy for cancer immunotherapy due to their robust... This study demonstrates the efficacy of combining macrophage-checkpoint inhibition with granulocytic myeloid-derived suppressor cell (G-MDSC) targeting as a...
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SubjectTerms	Animals Anticancer properties Biological Sciences Bone marrow Cancer immunotherapy CD47 Antigen Colony-stimulating factor CXCR2 protein Effectiveness Granulocytes Immunosuppression Immunotherapy Macrophage colony-stimulating factor Macrophages Melanoma Melanoma, Experimental Myeloid-Derived Suppressor Cells Phagocytosis Solid tumors Suppressor cells Synergism Tumor Microenvironment Tumors
Title	CXCR2 inhibition in G-MDSCs enhances CD47 blockade for melanoma tumor cell clearance
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