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IL-1β enables CNS access to CCR2hi monocytes and the generation of pathogenic cells through GM-CSF released by CNS

Alexandre Paré1,2, Benoit Mailhot1,2, Sébastien A Lévesque1,2

  • 1Centre de Recherche du Centre Hospitalier Universitaire de Québec, Université Laval, Québec, QC G1V 4G2, Canada.

Proceedings of the National Academy of Sciences of the United States of America
|January 24, 2018
PubMed

Insights

Targeting the IL-1β/IL-1R1 pathway blocks myeloid cell entry into the CNS, preventing neuroinflammation in models of multiple sclerosis (MS). This pathway is crucial for initiating and worsening central nervous system (CNS) inflammation.

Area of Science:

  • Neuroimmunology
  • Molecular and Cellular Biology

Background:

  • Autoimmune conditions like multiple sclerosis (MS) involve central nervous system (CNS) inflammation.
  • Interleukin-1 beta (IL-1β) plays a critical role in experimental autoimmune encephalomyelitis (EAE), an MS animal model.

Purpose of the Study:

  • To investigate the role of the IL-1β/IL-1R1 axis in myeloid cell infiltration and neuroinflammation during EAE.
  • To identify molecular targets for treating CNS autoimmune diseases.

Main Methods:

  • Utilized IL-1β-knockout mice to study resistance to EAE.
  • Examined myeloid cell transmigration across CNS endothelial cells (ECs).
  • Analyzed the expression of IL-1β, CCR2, GM-CSF, and CD4+ T cells in the spinal cord.

Main Results:

  • Interference with the IL-1β/IL-1R1 axis significantly reduced myeloid cell migration into the CNS.
  • IL-1β produced by inflammatory monocytes promotes their entry into the spinal cord before EAE onset.
  • Activated CNS ECs release GM-CSF, converting monocytes into antigen-presenting cells (APCs) that interact with CD4+ T cells, leading to neurotoxicity.

Conclusions:

  • IL-1β signaling is a critical regulator of myeloid cell entry into the CNS and subsequent neuroinflammation.
  • Targeting the IL-1β/IL-1R1 axis offers a potential therapeutic strategy for MS and other neuroinflammatory diseases.
Keywords:
autoimmunityblood–brain barrierexperimental autoimmune encephalomyelitisinterleukin-1βmultiple sclerosis

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