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S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production

INTRODUCTION: Splenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR(4)). Little is known about the functional relevance of S1PR(4) expression on those cells. METHODS: In this study, S1PR(4)-deficient mice were used to study the role of...

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Autores principales: Riese, Janik, Hähnel, Celine, Menz, Jonas, Hannemann, Maurice, Khabipov, Aydar, Lührs, Felix, Schulze, Tobias
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755867/
https://www.ncbi.nlm.nih.gov/pubmed/36532028
http://dx.doi.org/10.3389/fimmu.2022.1053490
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author Riese, Janik
Hähnel, Celine
Menz, Jonas
Hannemann, Maurice
Khabipov, Aydar
Lührs, Felix
Schulze, Tobias
author_facet Riese, Janik
Hähnel, Celine
Menz, Jonas
Hannemann, Maurice
Khabipov, Aydar
Lührs, Felix
Schulze, Tobias
author_sort Riese, Janik
collection PubMed
description INTRODUCTION: Splenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR(4)). Little is known about the functional relevance of S1PR(4) expression on those cells. METHODS: In this study, S1PR(4)-deficient mice were used to study the role of S1PR(4)-mediated S1P signaling in B cell motility in vitro and for the maintenance of the splenic architecture under steady state conditions as well as in polymicrobial abdominal sepsis in vivo. Finally, the impact of S1PR(4) deficiency on antibody production after immunization with T cell dependent antigens was assessed. RESULTS: Loss of S1PR(4) resulted in minor alterations of the splenic architecture concerning the presence of B cell follicles. After sepsis induction, the germinal center response was severely impaired in S1PR(4)-deficient animals. Splenic B cells showed reduced motility in the absence of S1PR(4). However, titres of specific antibodies showed only minor reductions in S1PR(4)-deficient animals. DISCUSSION: These observations suggest that S1P signaling mediated by S1PR(4) modifies chemokine-induced splenic B cell chemotaxis, thus modulating splenic microarchitecture, GC formation and T-cell dependent antibody production.
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spelling pubmed-97558672022-12-17 S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production Riese, Janik Hähnel, Celine Menz, Jonas Hannemann, Maurice Khabipov, Aydar Lührs, Felix Schulze, Tobias Front Immunol Immunology INTRODUCTION: Splenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR(4)). Little is known about the functional relevance of S1PR(4) expression on those cells. METHODS: In this study, S1PR(4)-deficient mice were used to study the role of S1PR(4)-mediated S1P signaling in B cell motility in vitro and for the maintenance of the splenic architecture under steady state conditions as well as in polymicrobial abdominal sepsis in vivo. Finally, the impact of S1PR(4) deficiency on antibody production after immunization with T cell dependent antigens was assessed. RESULTS: Loss of S1PR(4) resulted in minor alterations of the splenic architecture concerning the presence of B cell follicles. After sepsis induction, the germinal center response was severely impaired in S1PR(4)-deficient animals. Splenic B cells showed reduced motility in the absence of S1PR(4). However, titres of specific antibodies showed only minor reductions in S1PR(4)-deficient animals. DISCUSSION: These observations suggest that S1P signaling mediated by S1PR(4) modifies chemokine-induced splenic B cell chemotaxis, thus modulating splenic microarchitecture, GC formation and T-cell dependent antibody production. Frontiers Media S.A. 2022-12-02 /pmc/articles/PMC9755867/ /pubmed/36532028 http://dx.doi.org/10.3389/fimmu.2022.1053490 Text en Copyright © 2022 Riese, Hähnel, Menz, Hannemann, Khabipov, Lührs and Schulze https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Riese, Janik
Hähnel, Celine
Menz, Jonas
Hannemann, Maurice
Khabipov, Aydar
Lührs, Felix
Schulze, Tobias
S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
title S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
title_full S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
title_fullStr S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
title_full_unstemmed S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
title_short S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
title_sort s1pr(4) deficiency results in reduced germinal center formation but only marginally affects antibody production
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9755867/
https://www.ncbi.nlm.nih.gov/pubmed/36532028
http://dx.doi.org/10.3389/fimmu.2022.1053490
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