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Originally published online as doi:10.1189/jlb.0204114 on January 12, 2005

Published online before print January 12, 2005
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(Journal of Leukocyte Biology. 2005;77:496-502.)
© 2005 by Society for Leukocyte Biology

Inducible immune regulation following autoimmune disease in the immune-privileged eye

Nobuyoshi Kitaichi, Kenichi Namba and Andrew W. Taylor1

Schepens Eye Research Institute and the Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts

1 Correspondence: Schepens Eye Research Institute, 20 Staniford Street, Boston, MA 02114. E-mail: awtaylor{at}vision.eri.harvard.edu

The immune-privileged eye has the potential to induce regulatory immunity along with local mechanisms of immunosuppression. Rodent models of human autoimmune uveoretinitis [experimental autoimmune uveoretinitis (EAU)] recover without spontaneous recurrence of uveitis, which differs from uveitis in some humans. This raises the possibility that the mechanism of immune privilege in the rodent eye can reimpose itself during autoimmune uveoretinitis and re-establish tolerance to autoantigen. To investigate this possibility, we examined the spleens of EAU-recovered mice for regulatory immunity. We detected regulatory immunity when we adoptively transferred post-EAU spleen cells into other mice immunized for EAU. We could not detect this regulatory immunity in enucleated mice nor in naive mice. Moreover, unlike the mechanisms of anterior chamber-associated immune deviation, the suppression was only mediated by post-EAU CD4+ T cells, which required activation with autoantigen presented by post-EAU spleen antigen-presenting cells (APC). Our results demonstrate that when the immune-privileged ocular microenvironment recovers from an autoimmune response, it has influenced systemic immunity to retinal autoantigen by affecting APC and mediating induction of potential regulatory CD4+ T cells laying in wait in the post-EAU spleen for restimulation.

Key Words: regulatory T cells • ocular immunity




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