Inhibiting efferocytosis reverses macrophage-mediated immunosuppression in the leukemia microenvironment.

MERTK Mertk inhibitors acute myeloid leukemia efferocytosis leukemia associated macrophages leukemia microenvironment tumor micro environment (TME) tumor-associated macrophages

Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 17 01 2023
accepted: 20 02 2023
entrez: 24 3 2023
pubmed: 25 3 2023
medline: 28 3 2023
Statut: epublish

Résumé

Previous studies show that the spleen and bone marrow can serve as leukemia microenvironments in which macrophages play a significant role in immune evasion and chemoresistance. We hypothesized that the macrophage driven tolerogenic process of efferocytosis is a major contributor to the immunosuppressive leukemia microenvironment and that this was driven by aberrant phosphatidylserine expression from cell turnover and cell membrane dysregulation. Since MerTK is the prototypic efferocytosis receptor, we assessed whether the MerTK inhibitor MRX2843, which is currently in clinical trials, would reverse immune evasion and enhance immune-mediated clearance of leukemia cells. We found that inhibition of MerTK decreased leukemia-associated macrophage expression of M2 markers PD-L1, PD-L2, Tim-3, CD163 and Arginase-1 compared to vehicle-treated controls. Additionally, MerTK inhibition led to M1 macrophage repolarization including elevated CD86 and HLA-DR expression, and increased production of T cell activating cytokines, including IFN-β, IL-18, and IL-1β through activation of NF-κB. Collectively, this macrophage repolarization had downstream effects on T cells within the leukemia microenvironment, including decreased PD-1 These results demonstrate that MerTK inhibition using MRX2843 altered the leukemia microenvironment from tumor-permissive toward immune responsiveness to leukemia and culminated in improved immune-mediated clearance of AML.

Sections du résumé

Background
Previous studies show that the spleen and bone marrow can serve as leukemia microenvironments in which macrophages play a significant role in immune evasion and chemoresistance. We hypothesized that the macrophage driven tolerogenic process of efferocytosis is a major contributor to the immunosuppressive leukemia microenvironment and that this was driven by aberrant phosphatidylserine expression from cell turnover and cell membrane dysregulation.
Methods
Since MerTK is the prototypic efferocytosis receptor, we assessed whether the MerTK inhibitor MRX2843, which is currently in clinical trials, would reverse immune evasion and enhance immune-mediated clearance of leukemia cells.
Results
We found that inhibition of MerTK decreased leukemia-associated macrophage expression of M2 markers PD-L1, PD-L2, Tim-3, CD163 and Arginase-1 compared to vehicle-treated controls. Additionally, MerTK inhibition led to M1 macrophage repolarization including elevated CD86 and HLA-DR expression, and increased production of T cell activating cytokines, including IFN-β, IL-18, and IL-1β through activation of NF-κB. Collectively, this macrophage repolarization had downstream effects on T cells within the leukemia microenvironment, including decreased PD-1
Discussion
These results demonstrate that MerTK inhibition using MRX2843 altered the leukemia microenvironment from tumor-permissive toward immune responsiveness to leukemia and culminated in improved immune-mediated clearance of AML.

Identifiants

pubmed: 36960055
doi: 10.3389/fimmu.2023.1146721
pmc: PMC10027704
doi:

Substances chimiques

c-Mer Tyrosine Kinase EC 2.7.10.1
Hepatitis A Virus Cellular Receptor 2 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1146721

Subventions

Organisme : NCI NIH HHS
ID : P30 CA016086
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA046934
Pays : United States

Informations de copyright

Copyright © 2023 Cruz Cruz, Allison, Page, Jenkins, Wang, Earp, Frye, Graham, Verneris and Lee-Sherick.

Déclaration de conflit d'intérêts

SF and XW have filed a patent application describing MRX2843. HE, DG, XW, and SF are stockholders in Meryx, Inc. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest

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Auteurs

Joselyn Cruz Cruz (J)

Division of Pediatric Hematology, Oncology, and Bone Marrow Transplant, University of Colorado, Aurora, CO, United States.

Kristen C Allison (KC)

Division of Pediatric Hematology, Oncology, and Bone Marrow Transplant, University of Colorado, Aurora, CO, United States.

Lauren S Page (LS)

Division of Pediatric Hematology, Oncology, and Bone Marrow Transplant, University of Colorado, Aurora, CO, United States.

Alexis J Jenkins (AJ)

Division of Pediatric Hematology, Oncology, and Bone Marrow Transplant, University of Colorado, Aurora, CO, United States.

Xiaodong Wang (X)

Center for Integrative Chemical Biology and Drug Discovery, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

H Shelton Earp (HS)

Lineberger Comprehensive Cancer Center, Departments of Medicine and Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

Stephen V Frye (SV)

Center for Integrative Chemical Biology and Drug Discovery, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

Douglas K Graham (DK)

Department of Pediatrics, Emory University, Atlanta, GA, United States.

Michael R Verneris (MR)

Division of Pediatric Hematology, Oncology, and Bone Marrow Transplant, University of Colorado, Aurora, CO, United States.

Alisa B Lee-Sherick (AB)

Division of Pediatric Hematology, Oncology, and Bone Marrow Transplant, University of Colorado, Aurora, CO, United States.

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