ArticleBMC genetics2014
Determining immune components necessary for progression of pigment dispersing disease to glaucoma in DBA/2J mice.
Article in BMC genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Intraocular pressure induced blood retinal barrier compromise in mouse models and human glaucoma.Nature communications · 2026Article
- Pigment Dispersion Contributes to Ocular Immune Privilege in a DBA/2J Mouse Model of Pigmentary Glaucoma.Investigative ophthalmology & visual science · 2024Article
- Genetic Basis of Pigment Dispersion Syndrome and Pigmentary Glaucoma: An Update and Functional Insights.Genes · 2024Review
- The concept of gene therapy for glaucoma: the dream that has not come true yet.Neural regeneration research · 2024Review
- Angiopoietin-1 Knockout Mice as a Genetic Model of Open-Angle Glaucoma.Translational vision science & technology · 2020Article
- Molecular Genetics of Pigment Dispersion Syndrome and Pigmentary Glaucoma: New Insights into Mechanisms.Journal of ophthalmology · 2018Review
- Cleavage Speed and Blastomere Number in DBA/2J Compared with C57BL/6J Mouse Embryos.Journal of the American Association for Laboratory Animal Science : JAALAS · 2017Article
- Characterization of intraocular pressure pattern and changes of retinal ganglion cells in DBA2J glaucoma mice.International journal of ophthalmology · 2016Article
- Using genetic mouse models to gain insight into glaucoma: Past results and future possibilities.Experimental eye research · 2015Review
- Neurodegeneration severity can be predicted from early microglia alterations monitored in vivo in a mouse model of chronic glaucoma.Disease models & mechanisms · 2015Article
- Radiation pretreatment does not protect the rat optic nerve from elevated intraocular pressure-induced injury.Investigative ophthalmology & visual science · 2014Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe molecular mechanisms causing pigment dispersion syndrome (PDS) and the pathway(s) by which it progresses to pigmentary glaucoma are not known. Mutations in two melanosomal protein genes (Tyrp1(b) and Gpnmb(R150X)) are responsible for pigment dispersing iris disease, which progresses to intraocular pressure (IOP) elevation and subsequent glaucoma in DBA/2J mice. Melanosomal defects along with ocular immune abnormalities play a role in the propagation of pigment dispersion and progression to IOP elevation. Here, we tested the role of specific immune components in the progression of the iris disease and high IOP.
resultsWe tested the role of NK cells in disease etiology by genetically modifying the B6.D2-Gpnmb(R150X) Tyrp1(b) strain, which develops the same iris disease as DBA/2J mice. Our findings demonstrate that neither diminishing NK mediated cytotoxic activity (Prf1 mutation) nor NK cell depletion (Il2rg mutation) has any influence on the severity or timing of Gpnmb(R150X) Tyrp1(b) mediated iris disease. Since DBA/2J mice are deficient in CD94, an important immune modulator that often acts as an immune suppressor, we generated DBA/2J mice sufficient in CD94. Sufficiency of CD94 failed to alter either the iris disease or the subsequent IOP elevation. Additionally CD94 status had no detected effect on glaucomatous optic nerve damage.
conclusionOur previous data implicate immune components in the manifestation of pigment dispersion and/or IOP elevation in DBA/2J mice. The current study eliminates important immune components, specifically NK cells and CD94 deficiency, as critical in the progression of iris disease and glaucoma. This narrows the field of possible immune components responsible for disease progression.
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