IL-17 signaling induces iNOS+ microglia activation in retinal vascular diseases

Tian Zhou1, Yan Liu1, Ziqi Yang1

  • 1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, P. R. China.

Glia
|July 21, 2021
PubMed

Insights

Interleukin-17 (IL-17) triggers microglia activation and inducible nitric oxide synthase (iNOS) expression, driving retinal vascular diseases. Targeting the IL-17-STAT3-iNOS pathway offers new therapeutic strategies for retinopathy.

Area of Science:

  • Immunology
  • Ophthalmology
  • Neuroscience

Background:

  • Microglia activation and inflammation drive retinopathy pathogenesis.
  • Inducible nitric oxide synthase (iNOS) is crucial for microglia-mediated retinal injuries.
  • The mechanisms inducing microglia activation in retinal vascular diseases remain unclear.

Purpose of the Study:

  • To investigate the role of Interleukin-17 (IL-17) in microglia activation and retinal vascular disease development.
  • To elucidate the signaling pathway involved in IL-17-induced microglia activation.
  • To identify potential therapeutic targets for retinopathy.

Main Methods:

  • In vitro and in vivo experiments were conducted.
  • Analysis of microglia activation, iNOS expression, and STAT3 pathway.
  • Assessment of endothelial cell function, vascular leakage, and leukostasis.

Main Results:

  • IL-17 induced microglia activation and high iNOS expression.
  • IL-17 promoted retinal vascular disease progression.
  • The STAT3-iNOS pathway mediated IL-17-induced microglia activation, promoting vascular leakage and leukostasis via IL-6.

Conclusions:

  • IL-17 plays a critical role in microglia activation and retinopathy.
  • The IL-17-STAT3-iNOS pathway is essential for microglia-mediated retinal damage.
  • Targeting IL-17 or downstream effectors presents a novel therapeutic approach for retinal vascular diseases.