Celiac disease, lupus and multiple sclerosis are all conditions that turn the body’s immune system on itself, attacking its own nerves, tissues or other structures. Thanks to an unintentional discovery, glaucoma may soon be listed among their ranks.¹

The condition is the second leading cause of blindness in the world and, yet, its only modifiable risk factor is elevated intraocular pressure (IOP).² That could all change if this hypothesis plays out. Although the new concept is still in an early stage of research, a team of investigators from Massachusetts is speculating that glaucoma be filed under the autoimmune banner; blocking this autoimmune activity, they feel, could be the key to treatment and perhaps even prevention.¹

Using mice deficient in T-cells, B-cells or both and a process called adoptive cell transfer, the investigators have uncovered “compelling evidence that glaucomatous neurodegeneration is mediated in part by T-cells that are pre-sensitized by exposure to commensal microflora,” the report reads.

The researchers found that, in mice with glaucomatous damage, T-cells infiltrated the retina when IOP rose. Once these cells breach the blood-retina barrier, they target heat shock proteins. Researchers suspect that the T-cells attack the proteins because they perceive them as a threat due to prior exposure to bacterial heat shock proteins.^1,3

The team looked at T-cell activity in human patients with glaucoma as well and found they have five times the normal level of T-cells specific to heat shock proteins, suggesting that the same phenomenon may also contribute to the disease in humans, according to a Massachusetts Institute of Technology release.³

“This is the first report that, to our knowledge, describes an unexpected link and the sequential roles of elevated IOP, intact commensal microflora and activation of T-cell responses in the pathogenesis of glaucoma,” according to the researchers.¹