BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors

Autores
Sevdali, Eirini; Block, Violeta; Lataretu, Marie; Li, Huiying; Smulski, Cristian Roberto; Briem, Jana Susann; Heitz, Yannic; Fischer, Beate; Ramirez, Neftali Jose; Grimbacher, Bodo; Jäck, Hans-Martin; Voll, Reinhard E.; Hölzer, Martin; Schneider, Pascal; Eibel, Hermann
Año de publicación
2022
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Binding of BAFF to BAFFR activates in mature B cells PI3K/AKT signaling regulating protein synthesis, metabolic fitness, and survival. In humans, naive and memory B cells express the same levels of BAFFR, but only memory B cells seem to survive without BAFF. Here, we show that BAFF activates PI3K/AKT only in naive B cells and changes the expression of genes regulating migration, proliferation, growth, and survival. BAFF-induced PI3K/AKT activation requires direct interactions between BAFFR and the B cell antigen receptor (BCR) components CD79A and CD79B and is enhanced by the AKT coactivator TCL1A. Compared to memory B cells, naive B cells express more surface BCRs, which interact better with BAFFR than IgG or IgA, thus allowing stronger responses to BAFF. As ablation of BAFFR in naive and memory B cells causes cell death independent of BAFF-induced signaling, BAFFR seems to act also as an intrinsic factor for B cell survival.
Fil: Sevdali, Eirini. Albert Ludwigs University of Freiburg; Alemania
Fil: Block, Violeta. Albert Ludwigs University of Freiburg; Alemania
Fil: Lataretu, Marie. Universitat Jena; Alemania
Fil: Li, Huiying. Albert Ludwigs University of Freiburg; Alemania
Fil: Smulski, Cristian Roberto. Comisión Nacional de Energía Atómica. Centro Atómico Bariloche; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina
Fil: Briem, Jana Susann. Albert Ludwigs University of Freiburg; Alemania
Fil: Heitz, Yannic. Albert Ludwigs University of Freiburg; Alemania
Fil: Fischer, Beate. Albert Ludwigs University of Freiburg; Alemania
Fil: Ramirez, Neftali Jose. Albert Ludwigs University of Freiburg; Alemania
Fil: Grimbacher, Bodo. Albert Ludwigs University of Freiburg; Alemania
Fil: Jäck, Hans-Martin. Universitat Erlangen-Nuremberg; Alemania
Fil: Voll, Reinhard E.. Albert Ludwigs University of Freiburg; Alemania
Fil: Hölzer, Martin. Robert Koch Institut; Alemania
Fil: Schneider, Pascal. Universite de Lausanne; Suiza
Fil: Eibel, Hermann. Albert Ludwigs University of Freiburg; Alemania
Materia
BAFF
BAFFR
BCR
CP: IMMUNOLOGY
HUMAN MEMORY B CELLS
PI3K SIGNALING
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/216824
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/216824
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptorsSevdali, EiriniBlock, VioletaLataretu, MarieLi, HuiyingSmulski, Cristian RobertoBriem, Jana SusannHeitz, YannicFischer, BeateRamirez, Neftali JoseGrimbacher, BodoJäck, Hans-MartinVoll, Reinhard E.Hölzer, MartinSchneider, PascalEibel, HermannBAFFBAFFRBCRCP: IMMUNOLOGYHUMAN MEMORY B CELLSPI3K SIGNALINGhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Binding of BAFF to BAFFR activates in mature B cells PI3K/AKT signaling regulating protein synthesis, metabolic fitness, and survival. In humans, naive and memory B cells express the same levels of BAFFR, but only memory B cells seem to survive without BAFF. Here, we show that BAFF activates PI3K/AKT only in naive B cells and changes the expression of genes regulating migration, proliferation, growth, and survival. BAFF-induced PI3K/AKT activation requires direct interactions between BAFFR and the B cell antigen receptor (BCR) components CD79A and CD79B and is enhanced by the AKT coactivator TCL1A. Compared to memory B cells, naive B cells express more surface BCRs, which interact better with BAFFR than IgG or IgA, thus allowing stronger responses to BAFF. As ablation of BAFFR in naive and memory B cells causes cell death independent of BAFF-induced signaling, BAFFR seems to act also as an intrinsic factor for B cell survival.Fil: Sevdali, Eirini. Albert Ludwigs University of Freiburg; AlemaniaFil: Block, Violeta. Albert Ludwigs University of Freiburg; AlemaniaFil: Lataretu, Marie. Universitat Jena; AlemaniaFil: Li, Huiying. Albert Ludwigs University of Freiburg; AlemaniaFil: Smulski, Cristian Roberto. Comisión Nacional de Energía Atómica. Centro Atómico Bariloche; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; ArgentinaFil: Briem, Jana Susann. Albert Ludwigs University of Freiburg; AlemaniaFil: Heitz, Yannic. Albert Ludwigs University of Freiburg; AlemaniaFil: Fischer, Beate. Albert Ludwigs University of Freiburg; AlemaniaFil: Ramirez, Neftali Jose. Albert Ludwigs University of Freiburg; AlemaniaFil: Grimbacher, Bodo. Albert Ludwigs University of Freiburg; AlemaniaFil: Jäck, Hans-Martin. Universitat Erlangen-Nuremberg; AlemaniaFil: Voll, Reinhard E.. Albert Ludwigs University of Freiburg; AlemaniaFil: Hölzer, Martin. Robert Koch Institut; AlemaniaFil: Schneider, Pascal. Universite de Lausanne; SuizaFil: Eibel, Hermann. Albert Ludwigs University of Freiburg; AlemaniaElsevier2022-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/216824Sevdali, Eirini; Block, Violeta; Lataretu, Marie; Li, Huiying; Smulski, Cristian Roberto; et al.; BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors; Elsevier; Cell Reports; 39; 13; 6-2022; 1-502211-1247CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.celrep.2022.111019info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:04:37Zoai:ri.conicet.gov.ar:11336/216824instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 11:04:37.501CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
title BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
spellingShingle BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
Sevdali, Eirini
BAFF
BAFFR
BCR
CP: IMMUNOLOGY
HUMAN MEMORY B CELLS
PI3K SIGNALING
title_short BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
title_full BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
title_fullStr BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
title_full_unstemmed BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
title_sort BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors
dc.creator.none.fl_str_mv Sevdali, Eirini
Block, Violeta
Lataretu, Marie
Li, Huiying
Smulski, Cristian Roberto
Briem, Jana Susann
Heitz, Yannic
Fischer, Beate
Ramirez, Neftali Jose
Grimbacher, Bodo
Jäck, Hans-Martin
Voll, Reinhard E.
Hölzer, Martin
Schneider, Pascal
Eibel, Hermann
author Sevdali, Eirini
author_facet Sevdali, Eirini
Block, Violeta
Lataretu, Marie
Li, Huiying
Smulski, Cristian Roberto
Briem, Jana Susann
Heitz, Yannic
Fischer, Beate
Ramirez, Neftali Jose
Grimbacher, Bodo
Jäck, Hans-Martin
Voll, Reinhard E.
Hölzer, Martin
Schneider, Pascal
Eibel, Hermann
author_role author
author2 Block, Violeta
Lataretu, Marie
Li, Huiying
Smulski, Cristian Roberto
Briem, Jana Susann
Heitz, Yannic
Fischer, Beate
Ramirez, Neftali Jose
Grimbacher, Bodo
Jäck, Hans-Martin
Voll, Reinhard E.
Hölzer, Martin
Schneider, Pascal
Eibel, Hermann
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv BAFF
BAFFR
BCR
CP: IMMUNOLOGY
HUMAN MEMORY B CELLS
PI3K SIGNALING
topic BAFF
BAFFR
BCR
CP: IMMUNOLOGY
HUMAN MEMORY B CELLS
PI3K SIGNALING
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Binding of BAFF to BAFFR activates in mature B cells PI3K/AKT signaling regulating protein synthesis, metabolic fitness, and survival. In humans, naive and memory B cells express the same levels of BAFFR, but only memory B cells seem to survive without BAFF. Here, we show that BAFF activates PI3K/AKT only in naive B cells and changes the expression of genes regulating migration, proliferation, growth, and survival. BAFF-induced PI3K/AKT activation requires direct interactions between BAFFR and the B cell antigen receptor (BCR) components CD79A and CD79B and is enhanced by the AKT coactivator TCL1A. Compared to memory B cells, naive B cells express more surface BCRs, which interact better with BAFFR than IgG or IgA, thus allowing stronger responses to BAFF. As ablation of BAFFR in naive and memory B cells causes cell death independent of BAFF-induced signaling, BAFFR seems to act also as an intrinsic factor for B cell survival.
Fil: Sevdali, Eirini. Albert Ludwigs University of Freiburg; Alemania
Fil: Block, Violeta. Albert Ludwigs University of Freiburg; Alemania
Fil: Lataretu, Marie. Universitat Jena; Alemania
Fil: Li, Huiying. Albert Ludwigs University of Freiburg; Alemania
Fil: Smulski, Cristian Roberto. Comisión Nacional de Energía Atómica. Centro Atómico Bariloche; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte; Argentina
Fil: Briem, Jana Susann. Albert Ludwigs University of Freiburg; Alemania
Fil: Heitz, Yannic. Albert Ludwigs University of Freiburg; Alemania
Fil: Fischer, Beate. Albert Ludwigs University of Freiburg; Alemania
Fil: Ramirez, Neftali Jose. Albert Ludwigs University of Freiburg; Alemania
Fil: Grimbacher, Bodo. Albert Ludwigs University of Freiburg; Alemania
Fil: Jäck, Hans-Martin. Universitat Erlangen-Nuremberg; Alemania
Fil: Voll, Reinhard E.. Albert Ludwigs University of Freiburg; Alemania
Fil: Hölzer, Martin. Robert Koch Institut; Alemania
Fil: Schneider, Pascal. Universite de Lausanne; Suiza
Fil: Eibel, Hermann. Albert Ludwigs University of Freiburg; Alemania
description Binding of BAFF to BAFFR activates in mature B cells PI3K/AKT signaling regulating protein synthesis, metabolic fitness, and survival. In humans, naive and memory B cells express the same levels of BAFFR, but only memory B cells seem to survive without BAFF. Here, we show that BAFF activates PI3K/AKT only in naive B cells and changes the expression of genes regulating migration, proliferation, growth, and survival. BAFF-induced PI3K/AKT activation requires direct interactions between BAFFR and the B cell antigen receptor (BCR) components CD79A and CD79B and is enhanced by the AKT coactivator TCL1A. Compared to memory B cells, naive B cells express more surface BCRs, which interact better with BAFFR than IgG or IgA, thus allowing stronger responses to BAFF. As ablation of BAFFR in naive and memory B cells causes cell death independent of BAFF-induced signaling, BAFFR seems to act also as an intrinsic factor for B cell survival.
publishDate 2022
dc.date.none.fl_str_mv 2022-06
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/216824
Sevdali, Eirini; Block, Violeta; Lataretu, Marie; Li, Huiying; Smulski, Cristian Roberto; et al.; BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors; Elsevier; Cell Reports; 39; 13; 6-2022; 1-50
2211-1247
CONICET Digital
CONICET
url http://hdl.handle.net/11336/216824
identifier_str_mv Sevdali, Eirini; Block, Violeta; Lataretu, Marie; Li, Huiying; Smulski, Cristian Roberto; et al.; BAFFR activates PI3K/AKT signaling in human naive but not in switched memory B cells through direct interactions with B cell antigen receptors; Elsevier; Cell Reports; 39; 13; 6-2022; 1-50
2211-1247
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.celrep.2022.111019
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 12.982451

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