The healthy eye possesses a unique physiological and evolutionary adaptation that modifies the expression of immunity. This physiological adaptation is part of ocular immune privilege. The physiological role of immune privilege is to impart upon the eye immune protection that avoids the destructive side effects of immunogenic inflammation. Immunogenic inflammation associated with hypersensitivity reactions can grossly distort the visual axis resulting in blindness. Within the immune privileged ocular microenvironment, there are active mechanisms of immunoregulation and immunosuppression. This ocular system of immunoregulation and immunosuppression not only suppresses immunogenic inflammation, but also actively manipulates immunity to make the immune response itself immunosuppressive. By understanding the mechanism of ocular immunity, it will be possible to induce an immune response that promotes the elimination of pathogens and tumors without the consequences of immunogenic inflammation, prevent or cure ocular and other autoimmune diseases, and induce immunity that promotes acceptance of corneal, retinal, and other tissue transplants. The objectives of this proposal are to identify, characterize, and establish the role of constitutively produced factors that are immunoregulatory and immunosuppressive in the eye. We hypothesize that the such factors suppress the activation of innate and adaptive immunity associated with inflammation, while enhancing or maintaining expression of the characteristics associated with immune regulation or suppression. We will test this hypothesis by demonstrating that the ocular microenvironment promotes the alternative activation and induction of suppressor macrophages, that the ocular microenvironment promotes the induction of effector regulatory T cells, and that the nervous system makes a significant contribution to ocular immunity.

National Institute of Health (NIH)
National Eye Institute (NEI)
Research Project (R01)
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Anterior Eye Disease Study Section (AED)
Program Officer
Shen, Grace L
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Boston University
Schools of Medicine
United States
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Taylor, A W; Dixit, S; Yu, J (2015) Retinal Pigment Epithelial Cell Line Suppression of Phagolysosome Activation. Int J Ophthalmol Eye Sci Suppl 2:1-6
Lee, Darren J; Taylor, Andrew W (2015) Recovery from experimental autoimmune uveitis promotes induction of antiuveitic inducible Tregs. J Leukoc Biol 97:1101-9
Phan, Toan A; Taylor, Andrew W (2013) The neuropeptides ?-MSH and NPY modulate phagocytosis and phagolysosome activation in RAW 264.7 cells. J Neuroimmunol 260:9-16
Lee, Darren J; Taylor, Andrew W (2013) Both MC5r and A2Ar are required for protective regulatory immunity in the spleen of post-experimental autoimmune uveitis in mice. J Immunol 191:4103-11
Taylor, Andrew W (2013) Alpha-melanocyte stimulating hormone (?-MSH) is a post-caspase suppressor of apoptosis in RAW 264.7 macrophages. PLoS One 8:e74488
Taylor, Andrew W (2012) Primary Open-Angle Glaucoma: A Transforming Growth Factor-ýý Pathway-Mediated Disease. Am J Pathol 180:2201-4
Kawanaka, Norikuni; Taylor, Andrew W (2011) Localized retinal neuropeptide regulation of macrophage and microglial cell functionality. J Neuroimmunol 232:17-25
Taylor, Andrew W; Lee, Darren J (2011) The alpha-melanocyte stimulating hormone induces conversion of effector T cells into treg cells. J Transplant 2011:246856
Lee, Darren J; Taylor, Andrew W (2011) Following EAU recovery there is an associated MC5r-dependent APC induction of regulatory immunity in the spleen. Invest Ophthalmol Vis Sci 52:8862-7
Taylor, Andrew W; Kaplan, Henry J (2010) Ocular immune privilege in the year 2010: ocular immune privilege and uveitis. Ocul Immunol Inflamm 18:488-92

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