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Production and functions of IL-17 in microglia

Jun Kawanokuchi1, Kouki Shimizu, Atsumi Nitta

  • 1Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan.

Journal of Neuroimmunology
|January 1, 2008
PubMed

Insights

Interleukin-17 (IL-17) influences microglia, key cells in multiple sclerosis (MS) pathogenesis. This study reveals IL-17 boosts microglial production of inflammatory and neurotrophic factors, potentially driving autoimmune responses in the central nervous system.

Area of Science:

  • Neuroimmunology
  • Cellular immunology

Background:

  • Helper T cells producing Interleukin-17 (IL-17) are implicated in multiple sclerosis (MS) pathogenesis.
  • Microglia are central to the inflammatory processes in MS.

Purpose of the Study:

  • To investigate the effects of IL-17 on microglia.
  • To explore the role of microglia-derived IL-17 in central nervous system autoimmunity.

Main Methods:

  • Treatment of microglia with IL-17.
  • Measurement of microglial cytokine and molecule production.
  • Analysis of IL-17 production by microglia in response to other cytokines.

Main Results:

  • IL-17 treatment upregulated microglial production of IL-6, macrophage inflammatory protein-2, nitric oxide, adhesion molecules, and neurotrophic factors.
  • Microglia were found to produce IL-17 when stimulated with IL-23 or IL-1beta.
  • Microglia's capacity to produce IL-1beta and IL-23 suggests autocrine signaling for IL-17 induction.

Conclusions:

  • IL-17 modulates microglial function, promoting both inflammatory and potentially protective responses.
  • Microglia-derived IL-17, induced by autocrine IL-1beta and IL-23, may contribute to autoimmune pathogenesis in the central nervous system, including MS.

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