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IL-9 orchestrates immune regulation through CD39/CD73 dependent metabolic reprogramming.

Muhammed Ali Kizmaz1, Abdurrahman Simsek1, Tugce Bozkurt1

  • 1Bursa Uludağ University Faculty of Medicine, Department of Immunology, Bursa, Turkey.

International Immunopharmacology
|February 1, 2026
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Summary

Interleukin-9 (IL-9) enhances adenosine production by upregulating CD39 and CD73, promoting an immunosuppressive environment and impacting T-cell responses in inflammation.

Keywords:
ATP–adenosine metabolismCD39CD73IL-9ImmunometabolismPurinergic signaling

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Area of Science:

  • Immunology
  • Cellular Metabolism
  • Molecular Signaling

Background:

  • Extracellular adenosine triphosphate (ATP) is crucial in cellular energy and acts as a signaling molecule during inflammation.
  • Ectonucleotidases CD39 and CD73 hydrolyze extracellular ATP (eATP) to adenosine, regulating immune responses.
  • Interleukin-9 (IL-9) is a cytokine with known roles in immune modulation.

Purpose of the Study:

  • To investigate the effect of IL-9 on ATP-adenosine metabolism.
  • To determine how IL-9-mediated metabolic changes influence T-cell responses.
  • To explore the role of the CD39/CD73 axis in IL-9's immunomodulatory functions.

Main Methods:

  • Peripheral blood mononuclear cells (PBMCs) from healthy donors were used.
  • Flow cytometry (FC) and ELISA were employed to analyze phenotypic, functional, and metabolic changes.
  • Pharmacological inhibition of CD39 and CD73 was utilized to assess mechanistic roles.

Main Results:

  • IL-9 upregulated CD39 and CD73 expression, enhancing ATP to adenosine conversion.
  • This metabolic shift created an immunosuppressive microenvironment, particularly in regulatory T (Treg) cells.
  • IL-9 suppressed pro-inflammatory cytokines, increased anti-inflammatory cytokines, and inhibited T-cell proliferation.
  • Inhibition of CD39/CD73 largely reversed IL-9's effects on T-cells.

Conclusions:

  • IL-9 acts as a regulator of the CD39/CD73 pathway.
  • IL-9 influences immune responses by modulating ATP-adenosine metabolism.
  • This pathway is relevant in inflammatory and immune-mediated diseases with dysregulated purinergic signaling.