Myelin as an inflammatory mediator: Myelin interactions with complement, macrophages, and microglia in spinal cord injury

Timothy J. Kopper, John C. Gensel

Research output: Contribution to journalReview articlepeer-review

54 Scopus citations

Abstract

Spinal cord injury (SCI) triggers chronic intraspinal inflammation consisting of activated resident and infiltrating immune cells (especially microglia/macrophages). The environmental factors contributing to this protracted inflammation are not well understood; however, myelin lipid debris is a hallmark of SCI. Myelin is also a potent macrophage stimulus and target of complement-mediated clearance and inflammation. The downstream effects of these neuroimmune interactions have the potential to contribute to ongoing pathology or facilitate repair. This depends in large part on whether myelin drives pathological or reparative macrophage activation states, commonly referred to as M1 (proinflammatory) or M2 (alternatively) macrophages, respectively. Here we review the processes by which myelin debris may be cleared through macrophage surface receptors and the complement system, how this differentially influences macrophage and microglial activation states, and how the cellular functions of these myelin macrophages and complement proteins contribute to chronic inflammation and secondary injury after SCI.

Original languageEnglish
Pages (from-to)969-977
Number of pages9
JournalJournal of Neuroscience Research
Volume96
Issue number6
DOIs
StatePublished - Jun 2018

Bibliographical note

Publisher Copyright:
© 2017 Wiley Periodicals, Inc.

Keywords

  • C1q
  • CD36
  • CR3
  • Marco
  • TREM2
  • scavenger receptor AI/II

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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