Related Experiment Video
Updated: Sep 7, 2025

10:10
Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
Published on: February 15, 2022
1.5K
Mechanism of Secondary Glaucoma Development in HTLV-1 Uveitis
Yuan Zong1, Koju Kamoi1, Naoko Ando1
1Department of Ophthalmology and Visual Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Frontiers in Microbiology
|June 20, 2022
Summary
Human T-cell lymphotropic virus type 1 (HTLV-1) infection causes inflammation and cell proliferation in the eye, leading to secondary glaucoma. This study reveals how HTLV-1 damages trabecular meshwork cells, increasing intraocular pressure.
Area of Science:
- Ophthalmology
- Virology
- Immunology
Background:
- Human T-cell lymphotropic virus type 1 (HTLV-1) is linked to adult T-cell leukemia, myelopathy, and uveitis (HU).
- HTLV-1 uveitis (HU) is a common ocular inflammatory condition in endemic regions.
- Secondary glaucoma affects approximately 30% of HU patients, a significantly higher rate than in the general uveitis population.
Purpose of the Study:
- To investigate the in vitro mechanism by which HTLV-1 infection leads to secondary glaucoma in HU patients.
- To understand the cellular and molecular changes in trabecular meshwork cells following HTLV-1 exposure.
Main Methods:
- Human trabecular meshwork cells (HTMCs) were exposed to HTLV-1-producing T cells (MT-2).
- Infected HTMCs were analyzed for proliferation, NF-κB activation, and inflammatory cytokine/chemokine production.
Main Results:
- HTLV-1 infection induced proliferation of HTMCs.
- Nuclear factor (NF)-κB expression was activated in infected cells.
- Upregulated production of inflammatory cytokines (IL-6) and chemokines (CXCL10, CCL2, CXCL-8) was observed.
Conclusions:
- HTLV-1 infection of trabecular meshwork cells may cause secondary glaucoma by increasing tissue proliferation and decreasing aqueous humor outflow.
- Inflammatory cytokine and chemokine upregulation disrupts normal trabecular meshwork function, leading to elevated intraocular pressure and glaucoma.
Keywords:
HTLV-1 uveitisNF- kappa Bglaucomahuman T-cell leukemia virus type 1ocular hypertensionocular inflammationuveitisMore Related Videos
Related Concept Videos
Glaucoma: Overview
734
Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
734
Open Angle Glaucoma: Treatment
553
In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Drugs such as carbonic anhydrase inhibitors, α2- and...
553
Angle Closure Glaucoma: Treatment
660
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
660

