The frequency of follicular T helper cells differs in acute and chronic neuroinflammation

Abstract Beyond the major role of T cells in the pathogenesis of the autoimmune neuroinflammatory disorder multiple sclerosis (MS), recent studies have highlighted the impact of B cells on pathogenic inflammatory processes. Follicular T helper cells (Tfh) are essential for the promotion of B cell-dr...

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Main Authors: Adalie Baniahmad, Katharina Birkner, Johanna Görg, Julia Loos, Frauke Zipp, Beatrice Wasser, Stefan Bittner
Format: Article
Language:English
Published: Nature Publishing Group 2020-11-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-020-77588-9
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spelling doaj-c2d0199e2a4c4427b983c4c32fa8f1b32020-12-08T12:05:41ZengNature Publishing GroupScientific Reports2045-23222020-11-0110111110.1038/s41598-020-77588-9The frequency of follicular T helper cells differs in acute and chronic neuroinflammationAdalie Baniahmad0Katharina Birkner1Johanna Görg2Julia Loos3Frauke Zipp4Beatrice Wasser5Stefan Bittner6Department of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzDepartment of Neurology, Focus Program Translational Neuroscience (FTN) and Immunotherapy (FZI), Rhine Main Neuroscience Network (rmn2), University Medical Center of the Johannes Gutenberg University MainzAbstract Beyond the major role of T cells in the pathogenesis of the autoimmune neuroinflammatory disorder multiple sclerosis (MS), recent studies have highlighted the impact of B cells on pathogenic inflammatory processes. Follicular T helper cells (Tfh) are essential for the promotion of B cell-driven immune responses. However, their role in MS and its murine model, experimental autoimmune encephalomyelitis (EAE), is poorly investigated. A first step to achieving a better understanding of the contribution of Tfh cells to the disease is the consideration of Tfh cell localization in relation to genetic background and EAE induction method. Here, we investigated the Tfh cell distribution during disease progression in disease relevant organs in three different EAE models. An increase of Tfh frequency in the central nervous system (CNS) was observed during peak of C57BL/6 J EAE, paralleling chronic disease activity, whereas in relapsing–remitting SJL EAE mice Tfh cell frequencies were increased during remission. Furthermore, transferred Tfh-skewed cells polarized in vitro induced mild clinical symptoms in B6.Rag1−/− mice. We identified significantly higher levels of Tfh cells in the dura mater than in the CNS both in C57BL/6 and in SJL/J mice. Overall, our study emphasizes diverse, non-static roles of Tfh cells during autoimmune neuroinflammation.https://doi.org/10.1038/s41598-020-77588-9
collection DOAJ
language English
format Article
sources DOAJ
author Adalie Baniahmad
Katharina Birkner
Johanna Görg
Julia Loos
Frauke Zipp
Beatrice Wasser
Stefan Bittner
spellingShingle Adalie Baniahmad
Katharina Birkner
Johanna Görg
Julia Loos
Frauke Zipp
Beatrice Wasser
Stefan Bittner
The frequency of follicular T helper cells differs in acute and chronic neuroinflammation
Scientific Reports
author_facet Adalie Baniahmad
Katharina Birkner
Johanna Görg
Julia Loos
Frauke Zipp
Beatrice Wasser
Stefan Bittner
author_sort Adalie Baniahmad
title The frequency of follicular T helper cells differs in acute and chronic neuroinflammation
title_short The frequency of follicular T helper cells differs in acute and chronic neuroinflammation
title_full The frequency of follicular T helper cells differs in acute and chronic neuroinflammation
title_fullStr The frequency of follicular T helper cells differs in acute and chronic neuroinflammation
title_full_unstemmed The frequency of follicular T helper cells differs in acute and chronic neuroinflammation
title_sort frequency of follicular t helper cells differs in acute and chronic neuroinflammation
publisher Nature Publishing Group
series Scientific Reports
issn 2045-2322
publishDate 2020-11-01
description Abstract Beyond the major role of T cells in the pathogenesis of the autoimmune neuroinflammatory disorder multiple sclerosis (MS), recent studies have highlighted the impact of B cells on pathogenic inflammatory processes. Follicular T helper cells (Tfh) are essential for the promotion of B cell-driven immune responses. However, their role in MS and its murine model, experimental autoimmune encephalomyelitis (EAE), is poorly investigated. A first step to achieving a better understanding of the contribution of Tfh cells to the disease is the consideration of Tfh cell localization in relation to genetic background and EAE induction method. Here, we investigated the Tfh cell distribution during disease progression in disease relevant organs in three different EAE models. An increase of Tfh frequency in the central nervous system (CNS) was observed during peak of C57BL/6 J EAE, paralleling chronic disease activity, whereas in relapsing–remitting SJL EAE mice Tfh cell frequencies were increased during remission. Furthermore, transferred Tfh-skewed cells polarized in vitro induced mild clinical symptoms in B6.Rag1−/− mice. We identified significantly higher levels of Tfh cells in the dura mater than in the CNS both in C57BL/6 and in SJL/J mice. Overall, our study emphasizes diverse, non-static roles of Tfh cells during autoimmune neuroinflammation.
url https://doi.org/10.1038/s41598-020-77588-9
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