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IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab
Pemphigus is a life-threatening auto-immune blistering disease of the skin and mucous membrane that is caused by the production of auto-antibodies (auto-Abs) directed against adhesion proteins: desmoglein 1 and 3. We demonstrated in the “Ritux3” trial, the high efficacy of rituximab, an anti-CD20 re...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9330150/ https://www.ncbi.nlm.nih.gov/pubmed/35892674 http://dx.doi.org/10.3390/biomedicines10081774 |
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author | Font, Guillaume Walet-Balieu, Marie-Laure Petit, Marie Burel, Carole Maho-Vaillant, Maud Hébert, Vivien Chan, Philippe Fréret, Manuel Boyer, Olivier Joly, Pascal Calbo, Sébastien Bardor, Muriel Golinski, Marie-Laure |
author_facet | Font, Guillaume Walet-Balieu, Marie-Laure Petit, Marie Burel, Carole Maho-Vaillant, Maud Hébert, Vivien Chan, Philippe Fréret, Manuel Boyer, Olivier Joly, Pascal Calbo, Sébastien Bardor, Muriel Golinski, Marie-Laure |
author_sort | Font, Guillaume |
collection | PubMed |
description | Pemphigus is a life-threatening auto-immune blistering disease of the skin and mucous membrane that is caused by the production of auto-antibodies (auto-Abs) directed against adhesion proteins: desmoglein 1 and 3. We demonstrated in the “Ritux3” trial, the high efficacy of rituximab, an anti-CD20 recombinant monoclonal antibody, as the first-line treatment for pemphigus. However, 25% of patients relapsed during the six-month period after rituximab treatment. These early relapses were associated with a lower decrease in anti-desmoglein auto-Abs after the initial cycle of rituximab. The N-glycosylation of immunoglobulin-G (IgG) can affect their affinity for Fc receptors and their serum half-life. We hypothesized that the extended half-life of Abs could be related to modifications of IgG N-glycans. The IgG N-glycome from pemphigus patients and its evolution under rituximab treatment were analyzed. Pemphigus patients presented a different IgG N-glycome than healthy donors, with less galactosylated, sialylated N-glycans, as well as a lower level of N-glycans bearing an additional N-acetylglucosamine. IgG N-glycome from patients who achieved clinical remission was not different to the one observed at baseline. Moreover, our study did not identify the N-glycans profile as discriminating between relapsing and non-relapsing patients. We report that pemphigus patients present a specific IgG N-glycome. The changes observed in these patients could be a biomarker of autoimmunity susceptibility rather than a sign of inflammation. |
format | Online Article Text |
id | pubmed-9330150 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-93301502022-07-29 IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab Font, Guillaume Walet-Balieu, Marie-Laure Petit, Marie Burel, Carole Maho-Vaillant, Maud Hébert, Vivien Chan, Philippe Fréret, Manuel Boyer, Olivier Joly, Pascal Calbo, Sébastien Bardor, Muriel Golinski, Marie-Laure Biomedicines Article Pemphigus is a life-threatening auto-immune blistering disease of the skin and mucous membrane that is caused by the production of auto-antibodies (auto-Abs) directed against adhesion proteins: desmoglein 1 and 3. We demonstrated in the “Ritux3” trial, the high efficacy of rituximab, an anti-CD20 recombinant monoclonal antibody, as the first-line treatment for pemphigus. However, 25% of patients relapsed during the six-month period after rituximab treatment. These early relapses were associated with a lower decrease in anti-desmoglein auto-Abs after the initial cycle of rituximab. The N-glycosylation of immunoglobulin-G (IgG) can affect their affinity for Fc receptors and their serum half-life. We hypothesized that the extended half-life of Abs could be related to modifications of IgG N-glycans. The IgG N-glycome from pemphigus patients and its evolution under rituximab treatment were analyzed. Pemphigus patients presented a different IgG N-glycome than healthy donors, with less galactosylated, sialylated N-glycans, as well as a lower level of N-glycans bearing an additional N-acetylglucosamine. IgG N-glycome from patients who achieved clinical remission was not different to the one observed at baseline. Moreover, our study did not identify the N-glycans profile as discriminating between relapsing and non-relapsing patients. We report that pemphigus patients present a specific IgG N-glycome. The changes observed in these patients could be a biomarker of autoimmunity susceptibility rather than a sign of inflammation. MDPI 2022-07-22 /pmc/articles/PMC9330150/ /pubmed/35892674 http://dx.doi.org/10.3390/biomedicines10081774 Text en © 2022 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 Font, Guillaume Walet-Balieu, Marie-Laure Petit, Marie Burel, Carole Maho-Vaillant, Maud Hébert, Vivien Chan, Philippe Fréret, Manuel Boyer, Olivier Joly, Pascal Calbo, Sébastien Bardor, Muriel Golinski, Marie-Laure IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab |
title | IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab |
title_full | IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab |
title_fullStr | IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab |
title_full_unstemmed | IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab |
title_short | IgG N-glycosylation from Patients with Pemphigus Treated with Rituximab |
title_sort | igg n-glycosylation from patients with pemphigus treated with rituximab |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9330150/ https://www.ncbi.nlm.nih.gov/pubmed/35892674 http://dx.doi.org/10.3390/biomedicines10081774 |
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