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The role of the leukemia inhibitory factor receptor in neuroprotective signaling

Stephanie M Davis1, Keith R Pennypacker1

  • 1Center for Advanced Translational Stroke Science, Departments of Neurology and Neuroscience, University of Kentucky, Lexington, KY 40536, United States.

Pharmacology & Therapeutics
|August 23, 2017
PubMed

Insights

The leukemia inhibitory factor receptor (LIFR) plays a key role in neuroprotection and immune regulation. Targeting LIFR offers a promising therapeutic strategy for central nervous system disorders like stroke.

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Neurotropic cytokines signal via the leukemia inhibitory factor receptor (LIFR), a complex involving a 190kDa subunit and the gp130 subunit.
  • This signaling pathway is crucial for neurosurvival gene expression in neurons and oligodendrocytes.
  • LIFR activation also promotes an anti-inflammatory phenotype in immune cells.

Purpose of the Study:

  • To review the role of the LIFR in the central nervous system (CNS) and immune system.
  • To explore the therapeutic potential of targeting LIFR for brain pathologies, including stroke.
  • To highlight the understudied therapeutic applications of targeting the specific LIFR subunit.

Main Methods:

  • Literature review of studies on LIFR signaling.
  • Analysis of LIFR's role in neurodegenerative diseases and brain pathologies.
  • Examination of LIFR's impact on immune cell phenotype.

Main Results:

  • LIFR signaling mediates neuroprotective gene expression in CNS cells.
  • LIFR activation shifts immune cells towards an anti-inflammatory state.
  • Therapeutic targeting of LIFR remains underexplored despite its potential.

Conclusions:

  • The LIFR is a critical mediator of neurosurvival and immune modulation.
  • Targeting LIFR presents a novel therapeutic avenue for CNS disorders like stroke.
  • Further research into LIFR-specific therapies is warranted for brain pathologies.
Keywords:
Brain injuryCytokineInflammationSignal transduction

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