Macrophage recruitment in immune-privileged lens during capsule repair, necrotic fiber removal, and fibrosis

Yuting Li, Zhen Li, Yumeng Quan, Hongyun Cheng, Manuel A. Riquelme, Xiao Dong Li, Sumin Gu, Jean X. Jiang

Research output: Contribution to journalArticlepeer-review

Abstract

Emerging evidence challenges the lens as an immune-privileged organ. Here, we provide a direct mechanism supporting a role of macrophages in lens capsule rupture repair. Posterior lens capsule rupture in a connexin 50 and aquaporin 0 double-knockout mouse model resulted in lens tissue extrusion into the vitreous cavity with formation of a “tail-like” tissue containing delayed regressed hyaloid vessels, fibrotic tissue and macrophages at postnatal (P) 15 days. The macrophages declined after P 30 days with M2 macrophages detected inside the lens. By P 90 days, the “tail-like” tissue completely disappeared and the posterior capsule rupture was sealed with thick fibrotic tissue. Colony-stimulating factor 1 (CSF-1) accelerated capsule repair, whereas inhibition of the CSF-1 receptor delayed the repair. Together, these results suggest that lens posterior rupture leads to the recruitment of macrophages delivered by the regression delayed hyaloid vessels. CSF-1-activated M2 macrophages mediate capsule rupture repair and development of fibrosis.

Original languageEnglish (US)
Article number102533
JournaliScience
Volume24
Issue number6
DOIs
StatePublished - Jun 25 2021

Keywords

  • Immunology
  • Ophthalmology

ASJC Scopus subject areas

  • General

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