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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

ABSTRACT: Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

PROVIDER: PRJNA831273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18901606_1.fastq.gz	Fastqsanger.gz
	SRR18901606_2.fastq.gz	Fastqsanger.gz
	SRR18901607_1.fastq.gz	Fastqsanger.gz
	SRR18901607_2.fastq.gz	Fastqsanger.gz
	SRR18901608_1.fastq.gz	Fastqsanger.gz

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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca

Project description:How to identify subgroups of PCa patients for immune checkpoint therapy (ICT) remains not fully understood. Basic helix-loop-helix family member e22 (Bhlhe22) is upregulated in bone metastatic PCa and drives an immunosuppressive bone TME. Tumoral Bhlhe22 mediates the high expression of colony stimulating factor 2 (CSF2), which results in the infiltration of myeloid-derived suppressor cells (MDSCs) and prolonged immunocompromised T cell status. Here, we reveal the immunosuppressive mechanism of tumoral Bhlhe22 and provide a prospective ICT combination therapeutic for Bhlhe22+ PCa patients.

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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

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Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

Project description:Targeting Bhlhe22-dependent MDSCs infiltration relieves the immunosuppressive bone TME and reduces the ICT resistance in bone metastatic Pca [PC-3]

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Project description:Immune checkpoint inhibition (ICI) has revolutionized treatment in cancers that are naturally immunogenic by enabling infiltration of T cells into the tumor microenvironment (TME) and promoting cytotoxic signaling pathways. Tumors possessing complex immunosuppressive TME’s such as breast and pancreatic cancers present unique therapeutic obstacles as response rates to ICI remain low. Such tumors often recruit myeloid-derived suppressor cells (MDSCs) whose functioning prohibits both T-cell activation and infiltration. We attempted to sensitize these tumors to ICI using epigenetic modulation to target MDSC trafficking and function to foster a less immunosuppressive TME. We showed that combining a histone deacetylase inhibitor, entinostat (ENT), with anti–PD-1, anti–CTLA-4, [A1] [A2] or both, significantly improved tumor-free survival in both the HER2/neu transgenic breast cancer and the Panc02 metastatic pancreatic cancer mouse models. Using flow cytometry, gene expression profiling, and ex vivo functional assays, we characterized populations of tumor-infiltrating lymphocytes (TILs) and MDSCs, as well as their functional capabilities. We showed that addition of ENT to checkpoint inhibition led to significantly decreased suppression by granulocytic-MDSCs in the TME of both tumor types. We also demonstrated an increase in activated granzyme-B–producing CD8+ T effector cells in mice treated with combination therapy. Gene expression profiling of both MDSCs and TILs identified significant changes in immune-related pathways. In summary, addition of ENT to ICI significantly altered infiltration and function of innate immune cells, allowing for a more robust adaptive immune response. These findings provide a rationale for combination therapy in patients with immune-resistant tumors, including breast and pancreatic cancers.

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Project description:Myeloid-derived suppressor cells (MDSCs) are increased by tumor-derived factors and suppress anti-tumor immunity. MDSCs obtained at a late time point after tumor injection had stronger suppressive activity than MDSCs obtained at an early time point, as measured by T cell proliferation assays. To find factors in MDSCs that change during tumor growth, we analyzed gene expression profiles from MDSCs at different time points after tumor injection. We found that immune response-related genes were down-regulated, but pro-tumor function-related genes were up-regulated in both Mo-MDSCs and PMN-MDSCs at the late time point. Among differentially expressed genes, FK506 binding protein 51 (FKBP51), which is a member of the immunophilin protein family and plays a role in immunoregulation, was increased in the Mo- and PMN-MDSCs isolated from the late time points. Experiments using siRNA and a chemical inhibitor of FKBP51 revealed that FKBP51 contributes to the regulation of the suppressive function of MDSCs by increasing iNOS, ARG1, and ROS levels and enhancing NF-kappaB activity. Collectively, our data suggest that FKBP51 is a novel molecule that can be targeted to regulate the immunosuppressive function of MDSCs. To identify the factors that licensed MDSCs to be more suppressive as tumors grow, we analyzed gene expression profiles in the two subsets of MDSCs at different time points (3wks, 6wks) during tumor progression. CD11b+Ly-6C(high)Ly-6G(low) Mo-MDSCs and CD11b+Ly-6C(low)Ly-6G(high) PMN-MDSCs were sorted from pooled spleens of naÃ¯ve mice and Her-2/CT26 tumor-bearing mice. Total RNA was purified and gene expression was analyzed by the Affymetrix GeneChipÂ® Mouse Gene 1.0 ST Array.

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