Abstract
Purpose: :
Sympathetic ophthalmia, as an example of a bilateral disease in response to a unilateral injury, leads to our hypothesis that two eyes communicate with each other through an unknown mechanism. Evidence has been provided indicating the loss of the immune prelivige of an eye after injury and bilateral changes in the activation of several groups of cells in the retina after unilateral optic nerve crush. Our goal in this study was to determine if unilateral optic nerve crush can cause bilateral loss of the immune privilege of the eye.
Methods: :
Optic nerve crush was performed in wild-type (wt) B6 mice; 24 hours or 21 days after the induction of nerve damage, anterior chamber (a.c.) inoculation of ovalbumin (OVA) was performed in one eye (either ipsilateral or contralateral eye to the lesion). Seven days after the a.c. inoculation, the mice were immunized with OVA in Complete Freund's adjuvant (CFA) subcutaneously. One week later, the mice were tested for their ability to develop DTH (delayed type hypersensitivity) in response to an intradermal inoculation of OVA pulsed PEC (peritoneal exudates cells).
Results: :
Mice with optic nerve crush showed an increase in the DTH response to the ACAID (anterior chamber associated immune deviation) compared to non-sensitized control groups, regardless if the eye exposed to the antigen was ipsilateral or contralateral to the nerve crush. The loss of the bilateral immune privilege after unilateral injury was also observed when the antigen was inoculated in the a.c. 21 days after the optic nerve lesion.
Conclusions: :
The loss of the ocular immune privilege in the ipsilateral eye to the injury has been previously shown in models of surgical (penetrating) lesions and retinal laser burn. In this study, we show a bilateral loss of ACAID following a unilateral injury to the optic nerve both at 24 hr and 3 weeks after the optic nerve injury. In the future, we aim to elucidate the mechanisms that allow the communication between both eyes using this model by evaluating neural and immune signals as possible candidates.
Keywords: immune tolerance/privilege • optic nerve • neuropeptides