title: Effects of experimental ocular inflammation on ocular immune privilege.
abstract: OBJECTIVE
  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 microg lipopolysaccharide (LPS). For EAU induction, B10.A mice were immunized with 50 microg 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 eyes.
authors.affiliation: Schepens Eye Research Institute and Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114, USA.
authors.forename: K
authors.initials: K
authors.lastname: Ohta
authors.forename: B
authors.initials: B
authors.lastname: Wiggert
authors.forename: A W
authors.initials: AW
authors.lastname: Taylor
authors.forename: J W
authors.initials: JW
authors.lastname: Streilein
mesh_terms: D000818:Animals; D000869:Anterior Eye Segment / Q000276:immunology / Q000473:pathology; D001082:Aqueous Humor / Q000166:cytology / Q000502:physiology*; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D018916:Blood-Aqueous Barrier / Q000276:immunology; D005136:Eye Proteins; D006968:Hypersensitivity, Delayed / Q000276:immunology; D007249:Inflammation / Q000276:immunology; D007958:Leukocyte Count; D008070:Lipopolysaccharides; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D010047:Ovalbumin; D012173:Retinitis / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D012177:Retinol-Binding Proteins; D012486:Salmonella typhimurium; D013601:T-Lymphocytes / Q000276:immunology*; D014605:Uveitis / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D000099214:Retinol-Binding Proteins, Interstitial
chemical_list: D005136:Eye Proteins; D008070:Lipopolysaccharides; D010047:Ovalbumin; D012177:Retinol-Binding Proteins; D000099214:Retinol-Binding Proteins, Interstitial