Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation
Autor(a) principal: | |
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Data de Publicação: | 2013 |
Outros Autores: | , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/36087 http://dx.doi.org/10.4049/jimmunol.1202354 |
Resumo: | We have previously shown that regulatory T (Treg) cells that accumulate in the airways of allergic mice upregulate CC-chemokine receptor 4 (CCR4) expression. These Treg cells suppressed in vitro Th2 cell proliferation but not type 2 cytokine production. in the current study, using a well-established murine model of allergic lung disease or oral tolerance, we evaluated the in vivo activity of Treg cells in allergic airway inflammation with special focus on CCR4 function. We found that allergic, but not tolerant, mice treated with anti-CD25 Ab showed increased airway eosinophilia and IL-5- or IL-4-producing Th2 cells when compared with untreated mice. Notably, mice with CCR4 deficiency displayed an augmented airway allergic inflammation compared with wild-type or CCR2 knockout (KO) mice. the allergic phenotype of CCR4KO mice was similar to that observed in anti-CD25-treated mice. the exacerbated allergic inflammation of CCR4KO mice was directly associated with an impaired migration of Treg cells to airways and augmented frequency of pulmonary Th2 cells. Adoptive transfer of CD25(+) CD4(+) T cells expressing high levels of CCR4, but not CCR4KO CD25(+) CD4(+) T cells, attenuated the severe airway Th2 response of CCR4KO mice. Our results show that CCR4 is critically involved in the migration of Treg cells to allergic lungs that, in turn, attenuate airway Th2 activation and allergic eosinophilic inflammation. the Journal of Immunology, 2013, 190: 2614-2621. |
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Faustino, LucasFonseca, Denise Morais daTakenaka, Maisa Carla Silveira [UNIFESP]Mirotti, LucianaFlorsheim, Esther BorgesGuereschi, Marcia Grando [UNIFESP]Silva, Joao SantanaBasso, Alexandre Salgado [UNIFESP]Russo, MomtchiloUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)2016-01-24T14:31:25Z2016-01-24T14:31:25Z2013-03-15Journal of Immunology. Bethesda: Amer Assoc Immunologists, v. 190, n. 6, p. 2614-2621, 2013.0022-1767http://repositorio.unifesp.br/handle/11600/36087http://dx.doi.org/10.4049/jimmunol.120235410.4049/jimmunol.1202354WOS:000315657200019We have previously shown that regulatory T (Treg) cells that accumulate in the airways of allergic mice upregulate CC-chemokine receptor 4 (CCR4) expression. These Treg cells suppressed in vitro Th2 cell proliferation but not type 2 cytokine production. in the current study, using a well-established murine model of allergic lung disease or oral tolerance, we evaluated the in vivo activity of Treg cells in allergic airway inflammation with special focus on CCR4 function. We found that allergic, but not tolerant, mice treated with anti-CD25 Ab showed increased airway eosinophilia and IL-5- or IL-4-producing Th2 cells when compared with untreated mice. Notably, mice with CCR4 deficiency displayed an augmented airway allergic inflammation compared with wild-type or CCR2 knockout (KO) mice. the allergic phenotype of CCR4KO mice was similar to that observed in anti-CD25-treated mice. the exacerbated allergic inflammation of CCR4KO mice was directly associated with an impaired migration of Treg cells to airways and augmented frequency of pulmonary Th2 cells. Adoptive transfer of CD25(+) CD4(+) T cells expressing high levels of CCR4, but not CCR4KO CD25(+) CD4(+) T cells, attenuated the severe airway Th2 response of CCR4KO mice. Our results show that CCR4 is critically involved in the migration of Treg cells to allergic lungs that, in turn, attenuate airway Th2 activation and allergic eosinophilic inflammation. the Journal of Immunology, 2013, 190: 2614-2621.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Inst Biomed Sci, Dept Immunol, BR-05508900 São Paulo, BrazilUniv São Paulo, Sch Med Ribeirao Preto, Dept Biochem & Immunol, BR-14049900 Ribeirao Preto, SP, BrazilUniversidade Federal de São Paulo, São Paulo Sch Med, Dept Microbiol Immunol & Parasitol, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, São Paulo Sch Med, Dept Microbiol Immunol & Parasitol, BR-04023062 São Paulo, BrazilWeb of Science2614-2621engAmer Assoc ImmunologistsJournal of ImmunologyRegulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammationinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/360872022-09-27 11:31:15.101metadata only accessoai:repositorio.unifesp.br:11600/36087Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-09-27T14:31:15Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
title |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
spellingShingle |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation Faustino, Lucas |
title_short |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
title_full |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
title_fullStr |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
title_full_unstemmed |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
title_sort |
Regulatory T Cells Migrate to Airways via CCR4 and Attenuate the Severity of Airway Allergic Inflammation |
author |
Faustino, Lucas |
author_facet |
Faustino, Lucas Fonseca, Denise Morais da Takenaka, Maisa Carla Silveira [UNIFESP] Mirotti, Luciana Florsheim, Esther Borges Guereschi, Marcia Grando [UNIFESP] Silva, Joao Santana Basso, Alexandre Salgado [UNIFESP] Russo, Momtchilo |
author_role |
author |
author2 |
Fonseca, Denise Morais da Takenaka, Maisa Carla Silveira [UNIFESP] Mirotti, Luciana Florsheim, Esther Borges Guereschi, Marcia Grando [UNIFESP] Silva, Joao Santana Basso, Alexandre Salgado [UNIFESP] Russo, Momtchilo |
author2_role |
author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Faustino, Lucas Fonseca, Denise Morais da Takenaka, Maisa Carla Silveira [UNIFESP] Mirotti, Luciana Florsheim, Esther Borges Guereschi, Marcia Grando [UNIFESP] Silva, Joao Santana Basso, Alexandre Salgado [UNIFESP] Russo, Momtchilo |
description |
We have previously shown that regulatory T (Treg) cells that accumulate in the airways of allergic mice upregulate CC-chemokine receptor 4 (CCR4) expression. These Treg cells suppressed in vitro Th2 cell proliferation but not type 2 cytokine production. in the current study, using a well-established murine model of allergic lung disease or oral tolerance, we evaluated the in vivo activity of Treg cells in allergic airway inflammation with special focus on CCR4 function. We found that allergic, but not tolerant, mice treated with anti-CD25 Ab showed increased airway eosinophilia and IL-5- or IL-4-producing Th2 cells when compared with untreated mice. Notably, mice with CCR4 deficiency displayed an augmented airway allergic inflammation compared with wild-type or CCR2 knockout (KO) mice. the allergic phenotype of CCR4KO mice was similar to that observed in anti-CD25-treated mice. the exacerbated allergic inflammation of CCR4KO mice was directly associated with an impaired migration of Treg cells to airways and augmented frequency of pulmonary Th2 cells. Adoptive transfer of CD25(+) CD4(+) T cells expressing high levels of CCR4, but not CCR4KO CD25(+) CD4(+) T cells, attenuated the severe airway Th2 response of CCR4KO mice. Our results show that CCR4 is critically involved in the migration of Treg cells to allergic lungs that, in turn, attenuate airway Th2 activation and allergic eosinophilic inflammation. the Journal of Immunology, 2013, 190: 2614-2621. |
publishDate |
2013 |
dc.date.issued.fl_str_mv |
2013-03-15 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:31:25Z |
dc.date.available.fl_str_mv |
2016-01-24T14:31:25Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Journal of Immunology. Bethesda: Amer Assoc Immunologists, v. 190, n. 6, p. 2614-2621, 2013. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/36087 http://dx.doi.org/10.4049/jimmunol.1202354 |
dc.identifier.issn.none.fl_str_mv |
0022-1767 |
dc.identifier.doi.none.fl_str_mv |
10.4049/jimmunol.1202354 |
dc.identifier.wos.none.fl_str_mv |
WOS:000315657200019 |
identifier_str_mv |
Journal of Immunology. Bethesda: Amer Assoc Immunologists, v. 190, n. 6, p. 2614-2621, 2013. 0022-1767 10.4049/jimmunol.1202354 WOS:000315657200019 |
url |
http://repositorio.unifesp.br/handle/11600/36087 http://dx.doi.org/10.4049/jimmunol.1202354 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Journal of Immunology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
2614-2621 |
dc.publisher.none.fl_str_mv |
Amer Assoc Immunologists |
publisher.none.fl_str_mv |
Amer Assoc Immunologists |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764172051611648 |