Erratum to: Immune maintenance in glaucoma: boosting the body's own neuroprotective potential

Abstract

Glaucoma, a slow progressive neurodegenerative disorder associated with death of retinal ganglion cells and degeneration of their connected optic nerve fibers, has been classically linked to high intraocular pressure. Regardless of the primary risk factor, degeneration may continue, resulting in further loss of neurons and subsequent glaucomatous damage. During the past decade, scientists and clinicians began to accept that, in addition or as an alternative to fighting off the primary risk factor(s), there is a need to protect the tissue from the ongoing spread of damage-an approach collectively termed "neuroprotection." We found that the immune system, the body's own defense mechanism, plays a key role in the ability of the optic nerve and the retina to withstand glaucomatous conditions. This defense involves recruitment of both innate and adaptive immune cells that together create a protective niche and thereby halt disease progression. The spontaneous immune response might not be sufficient, and therefore, we suggest boosting it by immunization (with the appropriate antigen, at specific timing and predetermined optimal dosing) which may be developed into a suitable therapeutic vaccination to treat glaucoma. This view of immune system involvement in glaucoma will raise new challenges in glaucoma research, changing the way in which clinicians perceive the disease and the approach to therapy.[This corrects the article on p. in vol. .].

Fig. 1

Therapeutic vaccination for glaucoma: immune modulation to cease spread of damage. Following the initial insult, dying neurons create a hostile environment that includes apoptotic signals, free radicals and oxidative stress, toxic levels of glutamate, ionic imbalance, abnormal protein behavior, and deprivation of growth factors and neurotrophins. These factors and others, at different overlapping stages of disease progression, mediate further spread of damage and secondary degeneration, leading to the loss of neighboring, still healthy neurons. As a therapeutic approach, we suggest using an active or passive therapeutic vaccination that will lead to a regulated autoimmune response. In this way, autoimmune T cells, recognizing specific CNS antigens residing at the damaged retina, will participate in the recruitment and activation of macrophages, leading to the regulation of the local inflammation and restoration of homeostasis