The immune response in many areas of the body following trauma is inflammation followed by scarring and repair. In the eye, inflammation and scarring of tissues would greatly reduce and obscure the visual field of an individual. Therefore the eye has evolved into an immune privileged area, thereby inhibiting ocular inflammation. To study immune privilege we use an experimental model termed Anterior Chamber Associated Immune Deviation (ACAID). Recently, we have found that retinal laser burn (RLB) abolishes ACAID. This is of interest because lasers are gaining increase usage for treatment of glaucoma, myopia and Age-related macular degeneration. The purpose of this proposal is to understand the mechanism in RLB mice that lead to the loss of ACAID. We will use knowledge from previous studies that detail components (Aqueous humor, F4/80+ Antigen presenting cells and T-regulatory cells) of the immune system important for ocular immune privilege.
AIM 1 will identify changes in the aqueous humor environment that might contribute to the ability to induce ACAID in RLB mice compared to WT mice.
AIM 2 will determine if lack of immune privilege in the RLB mice is due to a defect in the F4/80+ ARC.
AIM 3 will determine the characteristics of T cells after RLB. This proposal is directly relevant to public health because its findings can lead to improved strategies for treating patients exposed to therapeutic or accidental laser exposure. Moreover, understanding the side effects of laser treatment to the retina will allow for more careful and controlled treatment of patients with diabetic retinopathy, uveitis and age related macular degeneration. Overall, the results of the studies may lead to translational studies that examine the changes in the ocular environment (aqueous humor) of humans who are treated for accidental laser burn, receive RLB in the course treatment for their eye disease or present with post eye trauma or eye surgery.
| Lucas, Kenyatta; Karamichos, Dimitris; Mathew, Rose et al. (2012) Retinal laser burn-induced neuropathy leads to substance P-dependent loss of ocular immune privilege. J Immunol 189:1237-42 |
