Cargando…

Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site

Proteinase 3 (PR3) is a neutrophil granulocyte enzyme and an autoantigen found in several forms of vasculitis. Due to the diagnostic and clinical importance of antibodies (Abs) to PR3, it is important to characterize the protein and the nature of its epitopes. Here, we have characterized PR3 monoclo...

Descripción completa

Detalles Bibliográficos
Autores principales: Zoega, Morten, Trier, Nicole Hartwig, Nejrup, Rikke Guldhammer, Chailyan, Anna, Friis, Tina, Højrup, Peter, Houen, Gunnar
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044823/
https://www.ncbi.nlm.nih.gov/pubmed/36975370
http://dx.doi.org/10.3390/antib12010023
_version_ 1784913441256898560
author Zoega, Morten
Trier, Nicole Hartwig
Nejrup, Rikke Guldhammer
Chailyan, Anna
Friis, Tina
Højrup, Peter
Houen, Gunnar
author_facet Zoega, Morten
Trier, Nicole Hartwig
Nejrup, Rikke Guldhammer
Chailyan, Anna
Friis, Tina
Højrup, Peter
Houen, Gunnar
author_sort Zoega, Morten
collection PubMed
description Proteinase 3 (PR3) is a neutrophil granulocyte enzyme and an autoantigen found in several forms of vasculitis. Due to the diagnostic and clinical importance of antibodies (Abs) to PR3, it is important to characterize the protein and the nature of its epitopes. Here, we have characterized PR3 monoclonal antibodies (MAbs) and disease-associated Abs and their dependency on the PR3 structure and modifications, especially interactions with α-defensins. Three MAbs (HYB 172-01, 172-04, 172-05), which bind to PR3 in its native and denatured forms and provide the disulphide bridges, were intact. α-1-antitrypsin (AT) binds to purified human neutrophil granulocyte PR3 and inhibits its proteolytic activity, towards a small synthetic peptide substrate and a large protein substrate (casein). AT also inhibited the binding of the three MAbs to PR3, indicating that they bind in a region affected by AT binding. However, the MAbs did not inhibit PR3 proteolytic activity with a small substrate, showing that they bound at the active site without restricting access to the substrate cleft. Patient-derived Abs showed essentially the same characteristics as the MAbs, with important implications for vasculitis diagnostics and pathophysiology. Current findings illustrate that PR3 epitopes depend on the three-dimensional structure of the PR3/defensin complex, and that the epitopes depend to a smaller or larger degree on PR3/defensin associations.
format Online
Article
Text
id pubmed-10044823
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-100448232023-03-29 Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site Zoega, Morten Trier, Nicole Hartwig Nejrup, Rikke Guldhammer Chailyan, Anna Friis, Tina Højrup, Peter Houen, Gunnar Antibodies (Basel) Article Proteinase 3 (PR3) is a neutrophil granulocyte enzyme and an autoantigen found in several forms of vasculitis. Due to the diagnostic and clinical importance of antibodies (Abs) to PR3, it is important to characterize the protein and the nature of its epitopes. Here, we have characterized PR3 monoclonal antibodies (MAbs) and disease-associated Abs and their dependency on the PR3 structure and modifications, especially interactions with α-defensins. Three MAbs (HYB 172-01, 172-04, 172-05), which bind to PR3 in its native and denatured forms and provide the disulphide bridges, were intact. α-1-antitrypsin (AT) binds to purified human neutrophil granulocyte PR3 and inhibits its proteolytic activity, towards a small synthetic peptide substrate and a large protein substrate (casein). AT also inhibited the binding of the three MAbs to PR3, indicating that they bind in a region affected by AT binding. However, the MAbs did not inhibit PR3 proteolytic activity with a small substrate, showing that they bound at the active site without restricting access to the substrate cleft. Patient-derived Abs showed essentially the same characteristics as the MAbs, with important implications for vasculitis diagnostics and pathophysiology. Current findings illustrate that PR3 epitopes depend on the three-dimensional structure of the PR3/defensin complex, and that the epitopes depend to a smaller or larger degree on PR3/defensin associations. MDPI 2023-03-13 /pmc/articles/PMC10044823/ /pubmed/36975370 http://dx.doi.org/10.3390/antib12010023 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zoega, Morten
Trier, Nicole Hartwig
Nejrup, Rikke Guldhammer
Chailyan, Anna
Friis, Tina
Højrup, Peter
Houen, Gunnar
Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site
title Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site
title_full Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site
title_fullStr Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site
title_full_unstemmed Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site
title_short Defensin Interactions in Relation to Monoclonal and Disease-Related Proteinase 3 Antibodies Binding at the Catalytic Site
title_sort defensin interactions in relation to monoclonal and disease-related proteinase 3 antibodies binding at the catalytic site
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044823/
https://www.ncbi.nlm.nih.gov/pubmed/36975370
http://dx.doi.org/10.3390/antib12010023
work_keys_str_mv AT zoegamorten defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite
AT triernicolehartwig defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite
AT nejruprikkeguldhammer defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite
AT chailyananna defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite
AT friistina defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite
AT højruppeter defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite
AT houengunnar defensininteractionsinrelationtomonoclonalanddiseaserelatedproteinase3antibodiesbindingatthecatalyticsite