Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection

Autores
Fermino, Marise L.; Dias, Fabrício C.; Lopes, Carla D.; Souza, Maria A.; Cruz, Ângela K.; Liu, Fu Tong; Chammas, Roger; Roque Barreira, Maria C.; Rabinovich, Gabriel Adrian; Bernardes, Emerson S.
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Galectin-3, an endogenous glycan-binding protein, plays essential roles during microbial infection by modulating innate and adaptive immunity. However, the role of galectin-3 within the CD4+CD25+Foxp3+ T regulatory (TREG) cell compartment has not yet been explored. Here, we found, in a model of Leishmania major infection, that galectin-3 deficiency increases the frequency of peripheral TREG cells both in draining lymph nodes (LNs) and sites of infection. These observations correlated with an increased severity of the disease, as shown by increased footpad swelling and parasite burden. Galectin-3-deficient (Lgals3−/−) TREG cells displayed higher CD103 expression, showed greater suppressive capacity, and synthesized higher amounts of IL-10 compared with their wild-type (WT) counterpart. Furthermore, both TREG cells and T effector (TEFF) cells from Lgals3−/− mice showed higher expression of Notch1 and the Notch target gene Hes-1. Interestingly, Notch signaling components were also altered in both TREG and TEFF cells from uninfected Lgals3−/− mice. Thus, endogenous galectin-3 regulates the frequency and function of CD4+CD25+Foxp3+ TREG cells and alters the course of L. major infection.
Fil: Fermino, Marise L.. Universidade de Sao Paulo; Brasil
Fil: Dias, Fabrício C.. Universidade de Sao Paulo; Brasil
Fil: Lopes, Carla D.. Universidade de Sao Paulo; Brasil
Fil: Souza, Maria A.. Universidade de Sao Paulo; Brasil
Fil: Cruz, Ângela K.. Universidade de Sao Paulo; Brasil
Fil: Liu, Fu Tong. University of California at Davis; Estados Unidos
Fil: Chammas, Roger. Universidade de Sao Paulo; Brasil
Fil: Roque Barreira, Maria C.. Universidade de Sao Paulo; Brasil
Fil: Rabinovich, Gabriel Adrian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Bernardes, Emerson S.. Universidade de Sao Paulo; Brasil
Materia
GALECTIN-3
IL-10
LEISHMANIA MAJOR
NOTCH SIGNALING
T REGULATORY (TREG) CELLS
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:11336/2356
Acceder
id CONICETDig_171fe5f48ac3da582c5e07f1f51e5828
oai_identifier_str oai:ri.conicet.gov.ar:11336/2356
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infectionFermino, Marise L.Dias, Fabrício C.Lopes, Carla D.Souza, Maria A.Cruz, Ângela K.Liu, Fu TongChammas, RogerRoque Barreira, Maria C.Rabinovich, Gabriel AdrianBernardes, Emerson S.GALECTIN-3IL-10LEISHMANIA MAJORNOTCH SIGNALINGT REGULATORY (TREG) CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Galectin-3, an endogenous glycan-binding protein, plays essential roles during microbial infection by modulating innate and adaptive immunity. However, the role of galectin-3 within the CD4+CD25+Foxp3+ T regulatory (TREG) cell compartment has not yet been explored. Here, we found, in a model of Leishmania major infection, that galectin-3 deficiency increases the frequency of peripheral TREG cells both in draining lymph nodes (LNs) and sites of infection. These observations correlated with an increased severity of the disease, as shown by increased footpad swelling and parasite burden. Galectin-3-deficient (Lgals3−/−) TREG cells displayed higher CD103 expression, showed greater suppressive capacity, and synthesized higher amounts of IL-10 compared with their wild-type (WT) counterpart. Furthermore, both TREG cells and T effector (TEFF) cells from Lgals3−/− mice showed higher expression of Notch1 and the Notch target gene Hes-1. Interestingly, Notch signaling components were also altered in both TREG and TEFF cells from uninfected Lgals3−/− mice. Thus, endogenous galectin-3 regulates the frequency and function of CD4+CD25+Foxp3+ TREG cells and alters the course of L. major infection.Fil: Fermino, Marise L.. Universidade de Sao Paulo; BrasilFil: Dias, Fabrício C.. Universidade de Sao Paulo; BrasilFil: Lopes, Carla D.. Universidade de Sao Paulo; BrasilFil: Souza, Maria A.. Universidade de Sao Paulo; BrasilFil: Cruz, Ângela K.. Universidade de Sao Paulo; BrasilFil: Liu, Fu Tong. University of California at Davis; Estados UnidosFil: Chammas, Roger. Universidade de Sao Paulo; BrasilFil: Roque Barreira, Maria C.. Universidade de Sao Paulo; BrasilFil: Rabinovich, Gabriel Adrian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; ArgentinaFil: Bernardes, Emerson S.. Universidade de Sao Paulo; BrasilWiley VCH Verlag2013-05-17info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/2356Fermino, Marise L.; Dias, Fabrício C.; Lopes, Carla D.; Souza, Maria A.; Cruz, Ângela K.; et al.; Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection; Wiley VCH Verlag; European Journal of Immunology; 43; 7; 17-5-2013; 1806-18170014-29801521-4141enginfo:eu-repo/semantics/altIdentifier/doi/10.1002/eji.201343381info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/eji.201343381/abstract;jsessionid=67113EC5897BBBED63DAF7E40BDBBE33.f03t04info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:47:38Zoai:ri.conicet.gov.ar:11336/2356instacron: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 09:47:39.75CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
title Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
spellingShingle Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
Fermino, Marise L.
GALECTIN-3
IL-10
LEISHMANIA MAJOR
NOTCH SIGNALING
T REGULATORY (TREG) CELLS
title_short Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
title_full Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
title_fullStr Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
title_full_unstemmed Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
title_sort Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection
dc.creator.none.fl_str_mv Fermino, Marise L.
Dias, Fabrício C.
Lopes, Carla D.
Souza, Maria A.
Cruz, Ângela K.
Liu, Fu Tong
Chammas, Roger
Roque Barreira, Maria C.
Rabinovich, Gabriel Adrian
Bernardes, Emerson S.
author Fermino, Marise L.
author_facet Fermino, Marise L.
Dias, Fabrício C.
Lopes, Carla D.
Souza, Maria A.
Cruz, Ângela K.
Liu, Fu Tong
Chammas, Roger
Roque Barreira, Maria C.
Rabinovich, Gabriel Adrian
Bernardes, Emerson S.
author_role author
author2 Dias, Fabrício C.
Lopes, Carla D.
Souza, Maria A.
Cruz, Ângela K.
Liu, Fu Tong
Chammas, Roger
Roque Barreira, Maria C.
Rabinovich, Gabriel Adrian
Bernardes, Emerson S.
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv GALECTIN-3
IL-10
LEISHMANIA MAJOR
NOTCH SIGNALING
T REGULATORY (TREG) CELLS
topic GALECTIN-3
IL-10
LEISHMANIA MAJOR
NOTCH SIGNALING
T REGULATORY (TREG) CELLS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Galectin-3, an endogenous glycan-binding protein, plays essential roles during microbial infection by modulating innate and adaptive immunity. However, the role of galectin-3 within the CD4+CD25+Foxp3+ T regulatory (TREG) cell compartment has not yet been explored. Here, we found, in a model of Leishmania major infection, that galectin-3 deficiency increases the frequency of peripheral TREG cells both in draining lymph nodes (LNs) and sites of infection. These observations correlated with an increased severity of the disease, as shown by increased footpad swelling and parasite burden. Galectin-3-deficient (Lgals3−/−) TREG cells displayed higher CD103 expression, showed greater suppressive capacity, and synthesized higher amounts of IL-10 compared with their wild-type (WT) counterpart. Furthermore, both TREG cells and T effector (TEFF) cells from Lgals3−/− mice showed higher expression of Notch1 and the Notch target gene Hes-1. Interestingly, Notch signaling components were also altered in both TREG and TEFF cells from uninfected Lgals3−/− mice. Thus, endogenous galectin-3 regulates the frequency and function of CD4+CD25+Foxp3+ TREG cells and alters the course of L. major infection.
Fil: Fermino, Marise L.. Universidade de Sao Paulo; Brasil
Fil: Dias, Fabrício C.. Universidade de Sao Paulo; Brasil
Fil: Lopes, Carla D.. Universidade de Sao Paulo; Brasil
Fil: Souza, Maria A.. Universidade de Sao Paulo; Brasil
Fil: Cruz, Ângela K.. Universidade de Sao Paulo; Brasil
Fil: Liu, Fu Tong. University of California at Davis; Estados Unidos
Fil: Chammas, Roger. Universidade de Sao Paulo; Brasil
Fil: Roque Barreira, Maria C.. Universidade de Sao Paulo; Brasil
Fil: Rabinovich, Gabriel Adrian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental (i); Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica; Argentina
Fil: Bernardes, Emerson S.. Universidade de Sao Paulo; Brasil
description Galectin-3, an endogenous glycan-binding protein, plays essential roles during microbial infection by modulating innate and adaptive immunity. However, the role of galectin-3 within the CD4+CD25+Foxp3+ T regulatory (TREG) cell compartment has not yet been explored. Here, we found, in a model of Leishmania major infection, that galectin-3 deficiency increases the frequency of peripheral TREG cells both in draining lymph nodes (LNs) and sites of infection. These observations correlated with an increased severity of the disease, as shown by increased footpad swelling and parasite burden. Galectin-3-deficient (Lgals3−/−) TREG cells displayed higher CD103 expression, showed greater suppressive capacity, and synthesized higher amounts of IL-10 compared with their wild-type (WT) counterpart. Furthermore, both TREG cells and T effector (TEFF) cells from Lgals3−/− mice showed higher expression of Notch1 and the Notch target gene Hes-1. Interestingly, Notch signaling components were also altered in both TREG and TEFF cells from uninfected Lgals3−/− mice. Thus, endogenous galectin-3 regulates the frequency and function of CD4+CD25+Foxp3+ TREG cells and alters the course of L. major infection.
publishDate 2013
dc.date.none.fl_str_mv 2013-05-17
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/11336/2356
Fermino, Marise L.; Dias, Fabrício C.; Lopes, Carla D.; Souza, Maria A.; Cruz, Ângela K.; et al.; Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection; Wiley VCH Verlag; European Journal of Immunology; 43; 7; 17-5-2013; 1806-1817
0014-2980
1521-4141
url http://hdl.handle.net/11336/2356
identifier_str_mv Fermino, Marise L.; Dias, Fabrício C.; Lopes, Carla D.; Souza, Maria A.; Cruz, Ângela K.; et al.; Galectin-3 negatively regulates the frequency and function of CD4+CD25+Foxp3+ regulatory T cells and influences the course of Leishmania major infection; Wiley VCH Verlag; European Journal of Immunology; 43; 7; 17-5-2013; 1806-1817
0014-2980
1521-4141
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1002/eji.201343381
info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/eji.201343381/abstract;jsessionid=67113EC5897BBBED63DAF7E40BDBBE33.f03t04
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
dc.publisher.none.fl_str_mv Wiley VCH Verlag
publisher.none.fl_str_mv Wiley VCH Verlag
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
_version_ 1842268873468936192
score 13.13397

Publicaciones similares