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Type I interferon sensing unlocks dormant adipocyte inflammatory potential.

Calvin C Chan1,2,3, Michelle S M A Damen3,4, Maria E Moreno-Fernandez3,4

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|June 4, 2020
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Type I interferon (IFN) signaling amplifies inflammation in fat cells, mimicking myeloid cells and worsening obesity. Inhibiting this pathway may offer new therapeutic strategies for metabolic diseases.

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Area of Science:

  • Immunology
  • Metabolic Disease Research
  • Cell Biology

Background:

  • White adipose tissue inflammation is key in obesity.
  • Mechanisms of adipocyte inflammation and its role in disease are not fully understood.

Purpose of the Study:

  • To investigate the role of type I interferon (IFN)/IFNα receptor (IFNAR) axis in adipocyte inflammation.
  • To explore the link between IFNAR signaling, adipocyte metabolism, and obesity pathogenesis.

Main Methods:

  • Activation and inhibition of type I IFN/IFNAR signaling in adipocytes.
  • Assessment of gene expression patterns and metabolic changes (glycolysis).
  • In vivo studies in mice and analysis of human adipocyte data.

Main Results:

  • Type I IFN/IFNAR axis activation enhances adipocyte inflammation and uncovers myeloid cell-like gene expression.
  • IFNβ signaling promotes adipocyte glycolysis; inhibiting glycolysis reduces IFNβ-driven inflammation.
  • Obesity induces type I IFN axis activation, contributing to pathogenesis in mice.
  • IFNβ effects are conserved in human adipocytes and linked to metabolic derangements.

Conclusions:

  • The type I IFN/IFNAR axis regulates shared inflammatory features in myeloid cells and adipocytes.
  • Adipocyte inflammation, driven by type I IFN/IFNAR signaling, is an underappreciated factor in obesity pathogenesis.
  • Targeting the type I IFN/IFNAR axis in adipocytes could be a therapeutic strategy for obesity-related metabolic diseases.