Macrophage recruitment in immune-privileged lens during capsule repair, necrotic fiber removal, and fibrosis.
Immunology
Ophthalmology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
25 Jun 2021
25 Jun 2021
Historique:
received:
15
01
2021
revised:
01
04
2021
accepted:
10
05
2021
entrez:
18
6
2021
pubmed:
19
6
2021
medline:
19
6
2021
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 34142044
doi: 10.1016/j.isci.2021.102533
pii: S2589-0042(21)00501-0
pmc: PMC8188486
doi:
Types de publication
Journal Article
Langues
eng
Pagination
102533Subventions
Organisme : NEI NIH HHS
ID : R01 EY012085
Pays : United States
Informations de copyright
© 2021 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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