These investigators propose to use genetically altered DBA/2J mice that are devoid of a subset of immune cells that mediate inflammatory responses. They will determine if the mice develop high IOP and glaucoma in the absence of these cells. Also, they will test if a specific DBA/2J gene predisposes to the inflammation and thereby confers susceptibility to IOP elevation.
Harmfully high intraocular pressure (IOP) is a major risk factor for glaucoma. Pigment dispersion syndrome (PDS) is a common condition that deposits abnormally liberated iris pigment into the pathway that drains the ocular fluid from the eye. In some cases, the deposited pigment harms the drain resulting in high IOP and glaucoma. Not all PDS progresses to high IOP and glaucoma suggesting that the pigment itself is not sufficient to induce high IOP. DBA/2J mice have pigment dispersion, mild intraocular inflammation and develop high IOP. We hypothesize that the pigment dispersion and inflammation cooperate to induce the high IOP in these mice. To test this hypothesis, we will use genetically altered DBA/2J mice that are devoid of a subset of immune cells that mediate inflammatory responses. We will determine if the mice develop high IOP and glaucoma in the absence of these cells. Also, we will test if a specific DBA/2J gene predisposes to the inflammation and thereby confers susceptibility to IOP elevation. Our studies may suggest new therapies to prevent progression from PDS to glaucoma by reducing inflammatory responses.
First published on: June 11, 2008
Last modified on: November 24, 2024