Signaling capacity of FcγRII isoforms in B-CLL cells

Autores
Gamberale, Romina; Fernández Calotti, Paula; Sanjurjo, Julieta; Arrossagaray, Guillermo; Avalos, Julio Sánchez; Geffner, Jorge Raúl; Giordano, Mirta Nilda
Año de publicación
2005
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Two main isoforms of Fcγ receptor II (CD32) have been described in humans: activatory FcγRIIA and inhibitory FcγRIIB. We have previously reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcγRIIB, as normal B lymphocytes, but also the myeloid FcγRIIA. The aim of this study was to evaluate the signaling capacity of both FcγRII isoforms in B-CLL cells. We found that FcγRIIA expressed by leukemic cells failed to induce Ca2+ mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcγRIIB effectively diminished BCR-triggered ERK1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcγRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcγRIIB, but not FcγRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo. © 2005 Elsevier Ltd. All rights reserved.
Fil: Gamberale, Romina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Fernández Calotti, Paula. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Sanjurjo, Julieta. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Arrossagaray, Guillermo. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Avalos, Julio Sánchez. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Giordano, Mirta Nilda. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Materia
B-Cll
FcΓRiia
FcΓRiib
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:11336/62421

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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Signaling capacity of FcγRII isoforms in B-CLL cellsGamberale, RominaFernández Calotti, PaulaSanjurjo, JulietaArrossagaray, GuillermoAvalos, Julio SánchezGeffner, Jorge RaúlGiordano, Mirta NildaB-CllFcΓRiiaFcΓRiibhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Two main isoforms of Fcγ receptor II (CD32) have been described in humans: activatory FcγRIIA and inhibitory FcγRIIB. We have previously reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcγRIIB, as normal B lymphocytes, but also the myeloid FcγRIIA. The aim of this study was to evaluate the signaling capacity of both FcγRII isoforms in B-CLL cells. We found that FcγRIIA expressed by leukemic cells failed to induce Ca2+ mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcγRIIB effectively diminished BCR-triggered ERK1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcγRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcγRIIB, but not FcγRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo. © 2005 Elsevier Ltd. All rights reserved.Fil: Gamberale, Romina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Fernández Calotti, Paula. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Sanjurjo, Julieta. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Arrossagaray, Guillermo. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Avalos, Julio Sánchez. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaFil: Giordano, Mirta Nilda. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; ArgentinaPergamon-Elsevier Science Ltd2005-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/62421Gamberale, Romina; Fernández Calotti, Paula; Sanjurjo, Julieta; Arrossagaray, Guillermo; Avalos, Julio Sánchez; et al.; Signaling capacity of FcγRII isoforms in B-CLL cells; Pergamon-Elsevier Science Ltd; Leukemia Research; 29; 11; 11-2005; 1277-12840145-2126CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.leukres.2005.04.008info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0145212605001736info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:57:46Zoai:ri.conicet.gov.ar:11336/62421instacron: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:34982025-09-03 09:57:46.359CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Signaling capacity of FcγRII isoforms in B-CLL cells
title Signaling capacity of FcγRII isoforms in B-CLL cells
spellingShingle Signaling capacity of FcγRII isoforms in B-CLL cells
Gamberale, Romina
B-Cll
FcΓRiia
FcΓRiib
title_short Signaling capacity of FcγRII isoforms in B-CLL cells
title_full Signaling capacity of FcγRII isoforms in B-CLL cells
title_fullStr Signaling capacity of FcγRII isoforms in B-CLL cells
title_full_unstemmed Signaling capacity of FcγRII isoforms in B-CLL cells
title_sort Signaling capacity of FcγRII isoforms in B-CLL cells
dc.creator.none.fl_str_mv Gamberale, Romina
Fernández Calotti, Paula
Sanjurjo, Julieta
Arrossagaray, Guillermo
Avalos, Julio Sánchez
Geffner, Jorge Raúl
Giordano, Mirta Nilda
author Gamberale, Romina
author_facet Gamberale, Romina
Fernández Calotti, Paula
Sanjurjo, Julieta
Arrossagaray, Guillermo
Avalos, Julio Sánchez
Geffner, Jorge Raúl
Giordano, Mirta Nilda
author_role author
author2 Fernández Calotti, Paula
Sanjurjo, Julieta
Arrossagaray, Guillermo
Avalos, Julio Sánchez
Geffner, Jorge Raúl
Giordano, Mirta Nilda
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv B-Cll
FcΓRiia
FcΓRiib
topic B-Cll
FcΓRiia
FcΓRiib
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Two main isoforms of Fcγ receptor II (CD32) have been described in humans: activatory FcγRIIA and inhibitory FcγRIIB. We have previously reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcγRIIB, as normal B lymphocytes, but also the myeloid FcγRIIA. The aim of this study was to evaluate the signaling capacity of both FcγRII isoforms in B-CLL cells. We found that FcγRIIA expressed by leukemic cells failed to induce Ca2+ mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcγRIIB effectively diminished BCR-triggered ERK1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcγRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcγRIIB, but not FcγRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo. © 2005 Elsevier Ltd. All rights reserved.
Fil: Gamberale, Romina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Fernández Calotti, Paula. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Sanjurjo, Julieta. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Arrossagaray, Guillermo. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Avalos, Julio Sánchez. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
Fil: Giordano, Mirta Nilda. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina; Argentina
description Two main isoforms of Fcγ receptor II (CD32) have been described in humans: activatory FcγRIIA and inhibitory FcγRIIB. We have previously reported that B cells from a subset of chronic lymphocytic leukemia (B-CLL) patients express not only FcγRIIB, as normal B lymphocytes, but also the myeloid FcγRIIA. The aim of this study was to evaluate the signaling capacity of both FcγRII isoforms in B-CLL cells. We found that FcγRIIA expressed by leukemic cells failed to induce Ca2+ mobilization or protein tyrosine phosphorylation, suggesting that the receptor is not functional. By contrast, FcγRIIB effectively diminished BCR-triggered ERK1 phosphorylation, which indicates that it is able to transduce inhibitory signals in B-CLL cells. Moreover, we found that FcγRIIB homoaggregation in either B-CLL or non-malignant tonsillar B cells did not result in apoptosis as was reported for murine B splenocytes. Together, these results show that FcγRIIB, but not FcγRIIA is biologically active in B-CLL cells and might influence leukemic cell physiology in vivo. © 2005 Elsevier Ltd. All rights reserved.
publishDate 2005
dc.date.none.fl_str_mv 2005-11
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/11336/62421
Gamberale, Romina; Fernández Calotti, Paula; Sanjurjo, Julieta; Arrossagaray, Guillermo; Avalos, Julio Sánchez; et al.; Signaling capacity of FcγRII isoforms in B-CLL cells; Pergamon-Elsevier Science Ltd; Leukemia Research; 29; 11; 11-2005; 1277-1284
0145-2126
CONICET Digital
CONICET
url http://hdl.handle.net/11336/62421
identifier_str_mv Gamberale, Romina; Fernández Calotti, Paula; Sanjurjo, Julieta; Arrossagaray, Guillermo; Avalos, Julio Sánchez; et al.; Signaling capacity of FcγRII isoforms in B-CLL cells; Pergamon-Elsevier Science Ltd; Leukemia Research; 29; 11; 11-2005; 1277-1284
0145-2126
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.leukres.2005.04.008
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0145212605001736
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
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
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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