Retina-arrestin specific CD8+ T cells are not implicated in HLA-A29-positive birdshot chorioretinitis

Retina-arrestin specific CD8+ T cells are not implicated in HLA-A29-positive birdshot chorioretinitis

Copyright © 2022. Published by Elsevier Inc.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 247(2023) vom: 25. Feb., Seite 109219
Auteur principal: Venema, W J (Auteur)
Autres auteurs: Hiddingh, S, Janssen, G M C, Ossewaarde-van Norel, J, van Loon, N Dam, de Boer, J H, van Veelen, P A, Kuiper, J J W
Format: Article en ligne
Langue:English
Publié: 2023
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't HLA-A29 antigen Arrestin HLA-A Antigens Peptides Autoantigens ERAP1 protein, human EC 3.4.11.- Aminopeptidases plus... Minor Histocompatibility Antigens ERAP2 protein, human
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100 1 |a Venema, W J  |e verfasserin  |4 aut 
245 1 0 |a Retina-arrestin specific CD8+ T cells are not implicated in HLA-A29-positive birdshot chorioretinitis 
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520 |a Copyright © 2022. Published by Elsevier Inc. 
520 |a BACKGROUND: HLA-A29-positive birdshot chorioretinitis (BCR) is an inflammatory eye disorder that is generally assumed to be caused by an autoimmune response to HLA-A29-presented peptides from retinal arrestin (SAG), yet the epitopes recognized by CD8+ T cells from patients remain to be identified 
520 |a OBJECTIVES: The identification of natural ligands of SAG presented by HLA-A29. To quantify CD8+ T cells reactive to antigenic SAG peptides presented by HLA-A29 in patients and controls 
520 |a METHODS: We performed mass-spectrometry based immunopeptidomics of HLA-A29 of antigen-presenting cell lines from patients engineered to express SAG. MHC-I Dextramer technology was utilised to determine expansion of antigen-specific CD8+ T cells reactive to SAG peptides in complex with HLA-A29 in a cohort of BCR patients, HLA-A29-positive controls, and HLA-A29-negative controls 
520 |a RESULTS: We report on the naturally presented antigenic SAG peptides identified by sequencing the HLA-A29 immunopeptidome of antigen-presenting cells of patients. We show that the N-terminally extended SAG peptide precursors can be trimmed in vitro by the antigen-processing aminopeptidases ERAP1 and ERAP2. Unexpectedly, no enhanced antigen engagement by CD8+ T cells upon stimulation with SAG peptides was observed in patients or HLA-A29-positive controls. Multiplexed HLA-A29-peptide dextramer profiling of a case-control cohort revealed that CD8+ T cells specific for these SAG peptides were neither detectable in peripheral blood nor in eye biopsies of patients 
520 |a CONCLUSIONS: Collectively, these findings demonstrate that SAG is not a CD8+ T cell autoantigen and sharply contrast the paradigm in the pathogenesis of BCR. Therefore, the mechanism by which HLA-A29 is associated with BCR does not involve SAG 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a HLA-A29 antigen  |2 NLM 
650 7 |a Arrestin  |2 NLM 
650 7 |a HLA-A Antigens  |2 NLM 
650 7 |a Peptides  |2 NLM 
650 7 |a Autoantigens  |2 NLM 
650 7 |a ERAP1 protein, human  |2 NLM 
650 7 |a EC 3.4.11.-  |2 NLM 
650 7 |a Aminopeptidases  |2 NLM 
650 7 |a EC 3.4.11.-  |2 NLM 
650 7 |a Minor Histocompatibility Antigens  |2 NLM 
650 7 |a ERAP2 protein, human  |2 NLM 
650 7 |a EC 3.4.11.-  |2 NLM 
700 1 |a Hiddingh, S  |e verfasserin  |4 aut 
700 1 |a Janssen, G M C  |e verfasserin  |4 aut 
700 1 |a Ossewaarde-van Norel, J  |e verfasserin  |4 aut 
700 1 |a van Loon, N Dam  |e verfasserin  |4 aut 
700 1 |a de Boer, J H  |e verfasserin  |4 aut 
700 1 |a van Veelen, P A  |e verfasserin  |4 aut 
700 1 |a Kuiper, J J W  |e verfasserin  |4 aut 
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