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Front Immunol. 2017 Oct 26;8:1383. doi: 10.3389/fimmu.2017.01383. eCollection 2017.

Toll-Like Receptor Ligands and Interferon-γ Synergize for Induction of Antitumor M1 Macrophages.

Frontiers in immunology

Elisabeth Müller, Panagiotis F Christopoulos, Sanjib Halder, Anna Lunde, Kahsai Beraki, Martin Speth, Inger Øynebråten, Alexandre Corthay

Affiliations

  1. Tumor Immunology Lab, Department of Pathology, Rikshospitalet, Oslo University Hospital, University of Oslo, Oslo, Norway.
  2. Department of Biosciences, University of Oslo, Oslo, Norway.

PMID: 29123526 PMCID: PMC5662546 DOI: 10.3389/fimmu.2017.01383

Abstract

Tumor-associated macrophages may either promote or suppress tumor growth depending on their activation status. Interferon-γ (IFN-γ) has been identified as a key factor for inducing tumoricidal M1 phenotype in macrophages. However, it remains unclear whether IFN-γ is sufficient or if additional stimuli are required. Here, we tested IFN-γ and a panel of toll-like receptor (TLR) agonists for the ability to activate murine macrophages toward a tumoricidal M1 phenotype. The following TLR ligands were used: TLR1/TLR2 agonist Pam3CSK4, TLR2/TLR6 agonist lipotechoic acid, TLR3 agonist poly(I:C), TLR4 agonist lipopolysaccharide (LPS), TLR5 agonist flagellin, TLR7 agonist CL264, and TLR9 agonist CpG. We used an

Keywords: cancer; immunotherapy; interferon-γ; macrophages; nitric oxide; toll-like receptors; tumoricidal

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