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Mouse brain microglia express interleukin-15 and its multimeric receptor complex functionally coupled to Janus kinase

U K Hanisch1, S A Lyons, M Prinz

  • 1Max Delbrück Center for Molecular Medicine, Cellular Neurosciences, Robert-Rössle-Strasse 10, 13122 Berlin-Buch, Germany. uh@nero.glia.mdc-berlin.de

Insights

Interleukin-15 (IL-15) and its receptor components are present in the mouse brain, specifically in microglia. IL-15 influences microglial function, suggesting a novel role in central nervous system (CNS) regulation.

Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Neuroscience

Background:

  • Interleukin-2 (IL-2) has suggested neuroregulatory roles, but its CNS expression is limited.
  • IL-2 and Interleukin-15 (IL-15) share receptor subunits (IL-2Rbeta and IL-2Rgamma) for signaling in immune cells.

Purpose of the Study:

  • To investigate the presence and function of IL-15 and its receptor system in the central nervous system (CNS).
  • To determine if microglia, the resident immune cells of the brain, express IL-15 and its associated receptors.

Main Methods:

  • RNA and protein detection methods were used to identify IL-15 and its receptor components in the mouse brain.
  • Single-cell analysis was performed to localize expression within microglia.
  • Functional assays assessed IL-15's effects on microglial nitric oxide production and cell growth.

Main Results:

  • Constitutive expression of IL-15, IL-15Ralpha, IL-2Rbeta, and IL-2Rgamma was detected in developing and adult mouse brains.
  • IL-15 and its receptor components were found to be expressed by microglia.
  • IL-15 signaling in microglia involves Janus kinase 1 (JAK1) activity.
  • Low doses of IL-15 modulated microglial nitric oxide production and supported cell growth, indicating autocrine functions.

Conclusions:

  • IL-15 is constitutively expressed in the brain and produced by microglia.
  • Microglial IL-15 may play a significant role in CNS functions, potentially mediating roles previously attributed to IL-2.

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