IOVS Annual Reviews: Social Science Suite
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Welge–Lüßen, U.
Right arrow Articles by Lütjen–Drecoll, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Welge–Lüßen, U.
Right arrow Articles by Lütjen–Drecoll, E.
(Investigative Ophthalmology and Visual Science. 1999;40:3209-3214.)
© 1999 by The Association for Research in Vision and Ophthalmology, Inc.

Loss of Anterior Chamber-Associated Immune Deviation (ACAID) in Aged Retinal Degeneration (rd) Mice

Ulrich Welge–Lüßen1, Caren Wilsch1, Thomas Neuhardt1, J. Wayne Streilein2 and Elke Lütjen–Drecoll1

1 From the Department of Anatomy II, Universitätsstraße 19, 91054 Erlangen, Germany; and 2 Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts.

PURPOSE. To determine whether the capacity to induce ACAID by antigen injection into the anterior chamber is altered in animals with genetically determined retinal degeneration and increased age.

METHODS. Anterior chamber–associated immune deviation (ACAID) induced by injection of ovalbumin into the anterior chamber of the eye was studied in three rodent strains with different forms of hereditary retinal degeneration (Royal College of Surgeon [RCS] rats, retinal degeneration [rd] mice, and Norrie–Disease [ND] mice) and in different age groups (age range, 1–23 months). The data were compared with those of age-matched controls. Aqueous humors of rd mice, RCS rats, and age-matched congenic controls were investigated for concentrations of transforming growth factor-ß2 (TGF-ß2) using enzyme-linked immunosorbent assay.

RESULTS. ACAID was readily induced in RCS rats and ND mice irrespective of amount of retinal degeneration or aging. In rd mice ACAID could be induced in young animals but not in animals more than 12 months of age. In old rd mice, loss of ACAID was accompanied by a marked reduction in total TGF-ß2 levels in aqueous humor.

CONCLUSIONS. Rd mice more than 1 year of age lose the capacity of the anterior chamber to support the induction of ACAID by intracameral injection of soluble protein antigen. Because loss of ACAID correlated with a decrease in TGF-ß2 concentration in aqueous humor, it is proposed that eyes of rd mice are unable to maintain an immunosuppressive microenvironment necessary for ACAID.




This article has been cited by other articles:


Home page
 J. Leukoc. Biol.Home page
A. D. Dick, D. Carter, M. Robertson, C. Broderick, E. Hughes, J. V. Forrester, and J. Liversidge
Control of myeloid activity during retinal inflammation
J. Leukoc. Biol., August 1, 2003; 74(2): 161 - 166.
[Abstract] [Full Text] [PDF]

Home page
 Br. J. Ophthalmol.Home page
D A Carter and A D Dick
Lipopolysaccharide/interferon-{gamma} and not transforming growth factor {beta} inhibits retinal microglial migration from retinal explant
Br. J. Ophthalmol., April 1, 2003; 87(4): 481 - 487.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by the Association for Research in Vision and Ophthalmology