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231226s2023 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2023.109817
|2 doi
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|a pubmed24n1371.xml
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|a (NLM)37925120
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|a (PII)S1521-6616(23)00580-6
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Paardekooper, Laurent M
|e verfasserin
|4 aut
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| 245 |
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|a Autoantibody subclass predominance is not driven by aberrant class switching or impaired B cell development
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|c 2023
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
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|2 rdacarrier
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| 500 |
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|a Date Completed 16.12.2023
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|a Date Revised 10.04.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.
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|a 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
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|a Journal Article
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| 650 |
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|a Autoimmune encephalitis
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| 650 |
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4 |
|a IgG4
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| 650 |
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|a Myasthenia gravis
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| 650 |
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4 |
|a Pemphigus
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| 650 |
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|a Plasma cells
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| 650 |
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|a Autoantibodies
|2 NLM
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| 650 |
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|a Immunoglobulin G
|2 NLM
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| 700 |
1 |
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|a Fillié-Grijpma, Yvonne E
|e verfasserin
|4 aut
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| 700 |
1 |
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|a van der Sluijs-Gelling, Alita J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zlei, Mihaela
|e verfasserin
|4 aut
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| 700 |
1 |
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|a van Doorn, Remco
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Vermeer, Maarten H
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Paunovic, Manuela
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Titulaer, Maarten J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a van der Maarel, Silvère M
|e verfasserin
|4 aut
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| 700 |
1 |
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|a van Dongen, Jacques J M
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Verschuuren, Jan J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Huijbers, Maartje G
|e verfasserin
|4 aut
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| 700 |
0 |
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|a T2B consortium
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 257(2023) vom: 22. Dez., Seite 109817
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:257
|g year:2023
|g day:22
|g month:12
|g pages:109817
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|u http://dx.doi.org/10.1016/j.clim.2023.109817
|3 Volltext
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