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Kouichi Ohta, Barbara Wiggert, Andrew W. Taylor, J. Wayne Streilein; Effects of Experimental Ocular Inflammation on Ocular Immune Privilege. Invest. Ophthalmol. Vis. Sci. 1999;40(9):2010-2018.
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purpose. To determine whether the inflammation of endotoxin-induced uveitis
(EIU) and experimental autoimmune uveoretinitis (EAU) alters key in
vivo and in vitro parameters of ocular immune privilege.
methods. For EIU induction, C3H/HeN mice received 200 μg lipopolysaccharide
(LPS). For EAU induction, B10.A mice were immunized with 50 μg
interphotoreceptor retinoid-binding protein (IRBP) mixed with complete
Freund’s adjuvant. Aqueous humor (AqH) was collected at periodic
intervals and assayed for leukocyte content and the ability to suppress
or enhance T-cell proliferation. Eyes with EAU were assessed for the
capacity to support anterior chamber (AC)-associated immune deviation
(ACAID) induction after injection of ovalbumin (OVA).
results. Inflammation within the anterior segment in EIU peaked at 12 to 24
hours and was detected from 10 days onward in EAU. In AqH of EIU,
protein content rose within 4 hours, followed by infiltrating
leukocytes. EIU AqH promptly lost its capacity to suppress T-cell
proliferation and became mitogenic for T cells. In AqH of EAU, protein
and leukocyte content rose at 11 days and continued to remain elevated
thereafter. Whereas 11-day EAU AqH failed to suppress T-cell
proliferation, AqH at later time points reacquired immunosuppressive
properties. Injection of OVA into the AC of eyes of mice with EAU
failed to induce ACAID.
conclusions. The intraocular inflammation of EIU and EAU disrupted important
parameters of immune privilege, ranging from breakdown of the
blood–ocular barrier, to loss of an immunosuppressive
microenvironment, to abrogation of ACAID. Because AqH from inflamed EAU
reacquired the ability to suppress T-cell proliferation, the authors
conclude that the capacity to regulate immune expression and
inflammation can be a property even of inflamed
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