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GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses
G-protein coupled receptors (GPCR) regulate 3’,5’-cyclic adenosine monophosphate (cAMP) levels in T cells. cAMP as ubiquitous second messenger is crucial for adequate physiology of T cells by mediating effector T cell (Teff) function as well as regulatory T cell (Treg)-mediated immunosuppression. Se...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9902724/ https://www.ncbi.nlm.nih.gov/pubmed/36761164 http://dx.doi.org/10.3389/fimmu.2022.1113348 |
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author | Krieg, Paula F. Sonner, Jana K. Kurelic, Roberta Engler, Jan Broder Scharenberg, Marlena F. Bauer, Simone Nikolaev, Viacheslav O. Friese, Manuel A. |
author_facet | Krieg, Paula F. Sonner, Jana K. Kurelic, Roberta Engler, Jan Broder Scharenberg, Marlena F. Bauer, Simone Nikolaev, Viacheslav O. Friese, Manuel A. |
author_sort | Krieg, Paula F. |
collection | PubMed |
description | G-protein coupled receptors (GPCR) regulate 3’,5’-cyclic adenosine monophosphate (cAMP) levels in T cells. cAMP as ubiquitous second messenger is crucial for adequate physiology of T cells by mediating effector T cell (Teff) function as well as regulatory T cell (Treg)-mediated immunosuppression. Several GPCRs have been identified to be crucial for Teff and Treg function. However, the role of the orphan, constitutively active Gs-coupled GPCR GPR52 is unknown. Here we show that GPR52 regulates cAMP levels in T cells but does not affect T cell function. We found that stimulation of transfected HEK cells or primary T cells with a GPR52 agonist results in a rise of intracellular cAMP. However, neither Gpr52 deficiency nor pharmacological modulation of GPR52 by antagonists or agonists affected T cell activation, differentiation, and proliferation or Treg-mediated immunosuppression. Moreover, Gpr52 deletion did not modify the clinical disease course of experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that a modulation of cAMP levels in T cells does not inevitably result in altered T cell function. While we could not identify an obvious role of GPR52 in in vitro T cell assays and in vivo CNS autoimmunity, it might regulate T cell function in a different context or affect the function of other GPR52-expressing cells. |
format | Online Article Text |
id | pubmed-9902724 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-99027242023-02-08 GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses Krieg, Paula F. Sonner, Jana K. Kurelic, Roberta Engler, Jan Broder Scharenberg, Marlena F. Bauer, Simone Nikolaev, Viacheslav O. Friese, Manuel A. Front Immunol Immunology G-protein coupled receptors (GPCR) regulate 3’,5’-cyclic adenosine monophosphate (cAMP) levels in T cells. cAMP as ubiquitous second messenger is crucial for adequate physiology of T cells by mediating effector T cell (Teff) function as well as regulatory T cell (Treg)-mediated immunosuppression. Several GPCRs have been identified to be crucial for Teff and Treg function. However, the role of the orphan, constitutively active Gs-coupled GPCR GPR52 is unknown. Here we show that GPR52 regulates cAMP levels in T cells but does not affect T cell function. We found that stimulation of transfected HEK cells or primary T cells with a GPR52 agonist results in a rise of intracellular cAMP. However, neither Gpr52 deficiency nor pharmacological modulation of GPR52 by antagonists or agonists affected T cell activation, differentiation, and proliferation or Treg-mediated immunosuppression. Moreover, Gpr52 deletion did not modify the clinical disease course of experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that a modulation of cAMP levels in T cells does not inevitably result in altered T cell function. While we could not identify an obvious role of GPR52 in in vitro T cell assays and in vivo CNS autoimmunity, it might regulate T cell function in a different context or affect the function of other GPR52-expressing cells. Frontiers Media S.A. 2023-01-24 /pmc/articles/PMC9902724/ /pubmed/36761164 http://dx.doi.org/10.3389/fimmu.2022.1113348 Text en Copyright © 2023 Krieg, Sonner, Kurelic, Engler, Scharenberg, Bauer, Nikolaev and Friese 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 Krieg, Paula F. Sonner, Jana K. Kurelic, Roberta Engler, Jan Broder Scharenberg, Marlena F. Bauer, Simone Nikolaev, Viacheslav O. Friese, Manuel A. GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses |
title | GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses |
title_full | GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses |
title_fullStr | GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses |
title_full_unstemmed | GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses |
title_short | GPR52 regulates cAMP in T cells but is dispensable for encephalitogenic responses |
title_sort | gpr52 regulates camp in t cells but is dispensable for encephalitogenic responses |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9902724/ https://www.ncbi.nlm.nih.gov/pubmed/36761164 http://dx.doi.org/10.3389/fimmu.2022.1113348 |
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