1. Academic Validation
  2. Schwann cell promotes macrophage recruitment through IL-17B/IL-17RB pathway in injured peripheral nerves

Schwann cell promotes macrophage recruitment through IL-17B/IL-17RB pathway in injured peripheral nerves

  • Cell Rep. 2024 Feb 27;43(2):113753. doi: 10.1016/j.celrep.2024.113753.
Yanju Huang 1 Liwen Wu 1 Yueshan Zhao 1 Jia Guo 2 Ruoyi Li 1 Suchen Ma 1 Zhengxin Ying 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Animal Biotech Breeding, Department of Nutrition and Health, College of Biological Sciences, China Agricultural University, Beijing 100193, China.
  • 2 National Institute of Biological Sciences, Beijing, No. 7 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China.
  • 3 State Key Laboratory of Animal Biotech Breeding, Department of Nutrition and Health, College of Biological Sciences, China Agricultural University, Beijing 100193, China; Chinese Institute for Brain Research, Beijing, No. 26 Science Park Road, Zhongguancun Life Science Park, Beijing 102206, China. Electronic address: [email protected].
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.

Keywords

CP: Immunology; CP: Neuroscience; IL-17; Schwann cell; macrophage; nerve injury; nerve regeneration.

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