Autoantibody subclass predominance is not driven by aberrant class switching or impaired B cell development

Autoantibody subclass predominance is not driven by aberrant class switching or impaired B cell development

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 257(2023) vom: 22. Dez., Seite 109817
1. Verfasser: Paardekooper, Laurent M (VerfasserIn)
Weitere Verfasser: Fillié-Grijpma, Yvonne E, van der Sluijs-Gelling, Alita J, Zlei, Mihaela, van Doorn, Remco, Vermeer, Maarten H, Paunovic, Manuela, Titulaer, Maarten J, van der Maarel, Silvère M, van Dongen, Jacques J M, Verschuuren, Jan J, Huijbers, Maartje G, T2B consortium
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2023
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Autoimmune encephalitis IgG4 Myasthenia gravis Pemphigus Plasma cells Autoantibodies Immunoglobulin G
Beschreibung
Zusammenfassung:Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.
A subset of autoimmune diseases is characterized by predominant pathogenic IgG4 autoantibodies (IgG4-AID). Why IgG4 predominates in these disorders is unknown. We hypothesized that dysregulated B cell maturation or aberrant class switching causes overrepresentation of IgG4+ B cells and plasma cells. Therefore, we compared the B cell compartment of patients from four different IgG4-AID with two IgG1-3-AID and healthy donors, using flow cytometry. Relative subset abundance at all maturation stages was normal, except for a, possibly treatment-related, reduction in immature and naïve CD5+ cells. IgG4+ B cell and plasma cell numbers were normal in IgG4-AID patients, however they had a (sub)class-independent 8-fold increase in circulating CD20-CD138+ cells. No autoreactivity was found in this subset. These results argue against aberrant B cell development and rather suggest the autoantibody subclass predominance to be antigen-driven. The similarities between IgG4-AID suggest that, despite displaying variable clinical phenotypes, they share a similar underlying immune profile
Beschreibung:Date Completed 16.12.2023
Date Revised 10.04.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2023.109817