Related Experiment Video
Updated: Jul 3, 2025

Neuron-Macrophage Co-cultures to Activate Macrophages Secreting Molecular Factors with Neurite Outgrowth Activity
Published on: March 30, 2018
Schwann cell promotes macrophage recruitment through IL-17B/IL-17RB pathway in injured peripheral nerves
Yanju Huang1, Liwen Wu1, Yueshan Zhao1
1State Key Laboratory of Animal Biotech Breeding, Department of Nutrition and Health, College of Biological Sciences, China Agricultural University, Beijing 100193, China.
Abstract:
Macrophage recruitment to the injured nerve initiates a cascade of events, including myelin debris clearance and nerve trophic factor secretion, which contribute to proper nerve tissue repair. However, the mechanism of macrophage recruitment is still unclear. Here, by comparing wild-type with Mlkl-/- and Sarm1-/- mice, two mouse strains with impaired myelin debris clearance after peripheral nerve injury, we identify interleukin-17B (IL-17B) as a key regulator of macrophage recruitment. Schwann-cell-secreted IL-17B acts in an autocrine manner and binds to IL-17 receptor B to promote macrophage recruitment, and global or Schwann-cell-specific IL-17B deletion reduces macrophage infiltration, myelin clearance, and axon regeneration. We also show that the IL-17B signaling pathway is defective in the injured central nerves. These results reveal an important role for Schwann cell autocrine signaling during Wallerian degeneration and point to potential mechanistic targets for accelerating myelin clearance and improving demyelinating disease.
Insights
Interleukin-17B (IL-17B) from Schwann cells drives macrophage recruitment for nerve repair. Blocking IL-17B impairs myelin clearance and axon regeneration, offering targets for demyelinating diseases.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Macrophage recruitment is crucial for nerve repair following injury.
- The precise mechanisms governing macrophage recruitment remain incompletely understood.
- Wallerian degeneration involves myelin debris clearance and nerve regeneration.
Purpose of the Study:
- To elucidate the molecular mechanisms regulating macrophage recruitment after peripheral nerve injury.
- To identify key signaling pathways involved in Schwann cell-mediated nerve repair.
- To investigate the role of IL-17B in macrophage infiltration and myelin clearance.
Main Methods:
- Comparative analysis of wild-type, Mlkl-/-, and Sarm1-/- mice after peripheral nerve injury.
- Assessment of macrophage infiltration, myelin debris clearance, and axon regeneration.
- Investigation of the IL-17B signaling pathway in Schwann cells and injured nerves.
Main Results:
- Interleukin-17B (IL-17B) was identified as a critical regulator of macrophage recruitment.
- Schwann cell-secreted IL-17B acts via IL-17 receptor B in an autocrine manner.
- Deletion of IL-17B, globally or in Schwann cells, reduced macrophage infiltration, myelin clearance, and axon regeneration.
- The IL-17B signaling pathway was found to be defective in injured central nerves.
Conclusions:
- Schwann cell autocrine IL-17B signaling plays a vital role in Wallerian degeneration.
- IL-17B is a key mediator of macrophage recruitment essential for nerve repair.
- Targeting the IL-17B pathway may accelerate myelin clearance and benefit demyelinating diseases.
Related Concept Videos
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Neurogenesis and Regeneration of Nervous Tissue

