IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

(Investigative Ophthalmology and Visual Science. 2006;47:2027-2035.)
© 2006 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.05-0984
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 ISI Web of Science
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 Google Scholar
Google Scholar
Right arrow Articles by Guyver, C. J.
Right arrow Articles by Nicholson, L. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Guyver, C. J.
Right arrow Articles by Nicholson, L. B.

Mapping Immune Responses to mRBP-3 1-16 Peptide with Altered Peptide Ligands

Carly J. Guyver,1 David A. Copland,2 Claudia J. Calder,1 Alessandro Sette,3 John Sidney,3 Andrew D. Dick,2 and Lindsay B. Nicholson1,2

1From the Department of Cellular and Molecular Medicine, School of Medical Sciences and 2Unit of Ophthalmology, Department of Clinical Sciences South Bristol, University of Bristol, Bristol, United Kingdom; and 3La Jolla Institute for Allergy and Immunology, San Diego, California.

PURPOSE. Experimental autoimmune uveoretinitis (EAU) can be induced in C57BL/6 mice (I-Ab) using human retinoid-binding protein-3 (hRBP-3, previously IRBP) residues 1-20. This study of a truncated murine peptide (mRBP-3 1-16) was conducted to determine its pathogenic potential and to characterize partially its interaction with specific T cells.

METHODS. After immunization with mRBP-3 1-16 or hRBP-3 1-20, EAU was assessed by immunohistochemistry. The immune response was assessed by tritiated thymidine incorporation and cytokine production analyzed by enzyme-linked immunosorbent assay (ELISA). T-cell receptor (TCR)- and major histocompatibility complex (MHC)-binding of mRBP-3 1-16 was studied by modeling and by using altered peptide ligands (APLs) and T-cell clones.

RESULTS. mRBP-3 1-16 induced EAU in C57BL/6 mice, with severity and kinetics comparable to that after immunization with hRBP-3 1-20. T cells taken from mice immunized with mRBP-3 1-16 had a Th1 phenotype and proliferated in response to reactivation with mRBP-3 1-16, hRBP-3 1-20, or mRBP-3 1-16 APLs. mRBP-3 1-16 APLs elicited at least five distinct patterns of reactivity when tested with the mRBP-3 1-16-reactive T-cell clones.

CONCLUSIONS. mRBP-3 1-16 immunizes and causes EAU in C57BL/6 mice. The studies using T-cell clones and APLs demonstrate that the immune response to mRBP-3 1-16 is drawn from a diverse population of antigen-specific T cells with a Th1 phenotype. Modeling and analysis of clones indicate that nonpathogenic T cells of an mRBP-3 1-16-reactive T-cell line recognize the peptide in a single register.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the Association for Research in Vision and Ophthalmology