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Concomitant type I IFN and M-CSF signaling reprograms monocyte differentiation and drives pro-tumoral arginase

Yuanyuan Tong1, Luyang Zhou2, Limin Yang1

  • 1State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center of Nanjing University, Nanjing 210061, China.

Ebiomedicine
|December 12, 2018
PubMed
Abstract

Insights

Type I interferon (IFN) therapy shows dual effects on tumor-associated macrophages (TAMs). While IFN restricts monocyte differentiation into TAMs, it also induces arginase-1, limiting therapeutic success in solid tumors.

Area of Science:

  • Immunology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Type I interferon (IFN)-based therapies have limited efficacy against solid tumors.
  • The impact of IFN on tumor-associated macrophages (TAMs) and its role in therapeutic outcomes remain poorly understood.

Purpose of the Study:

  • To investigate the effects of IFN on monocytes and TAMs within the tumor microenvironment.
  • To elucidate the mechanisms underlying IFN's actions on TAM differentiation and function.

Main Methods:

  • Utilized a transplantable mouse tumor model (LLC) treated with an IFN-inducer, poly(I:C).
  • Analyzed tumor-infiltrating monocytes and TAMs.
  • Employed in vitro culture systems to study direct IFN effects on differentiating monocytes.

Main Results:

  • Poly(I:C)-induced IFN inhibited the differentiation of Ly6C+ monocytes into TAMs via miR-155-mediated suppression of M-CSF receptor.
  • IFN treatment unexpectedly induced arginase-1 (Arg1) expression in monocytes through prolonged STAT3 and elevated M-CSF signaling.
  • ARG1 induction counteracted the therapeutic benefits of IFN by suppressing CD8+ T cell responses.

Conclusions:

  • IFN exhibits opposing actions on the TAM compartment: inhibiting differentiation while inducing arginase-1.
  • IFN-mediated immunoregulation has complex implications for cancer therapy, suggesting arginase inhibition as a potential synergistic strategy.
Keywords:
Anti-tumor immunityArginaseM-CSFMonocyte maturationTumor-associated macrophagesType I IFN

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