Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production

Detalhes bibliográficos
Autor(a) principal: Postol, Edilberto
Data de Publicação: 2008
Outros Autores: Meyer, Andre, Cardillo, Fabiola, Alencar, Raquel de, Pessina, Daniel, Nihei, Jorge, Mariano, Mario [UNIFESP], Mengel, Jose
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/30917
http://dx.doi.org/10.1111/j.1365-2567.2008.02835.x
Resumo: The role of natural killer (NK) T cells in the development of lupus-like disease in mice is still controversial. We treated NZB/W mice with anti-NK1.1 monoclonal antibodies (mAbs) and our results revealed that administration of either an irrelevant immunoglobulin G2a (IgG2a) mAb or an IgG2a anti-NK1.1 mAb increased the production of anti-dsDNA antibodies in young NZB/W mice. However, the continuous administration of an anti-NK1.1 mAb protected aged NZB/W mice from glomerular injury, leading to prolonged survival and stabilization of the proteinuria. Conversely, the administration of the control IgG2a mAb led to an aggravation of the lupus-like disease. Augmented titres of anti-dsDNA in NZB/W mice, upon IgG2a administration, correlated with the production of BAFF/BLyS by dendritic, B and T cells. Treatment with an anti-NK1.1 mAb reduced the levels of interleukin-16, produced by T cells, in spleen cell culture supernatants from aged NZB/W. Adoptive transfer of NK T cells from aged to young NZB/W accelerated the production of anti-dsDNA in recipient NZB/W mice, suggesting that NK T cells from aged NZB/W are endowed with a B-cell helper activity. in vitro studies, using purified NK T cells from aged NZB/W, showed that these cells provided helper B-cell activity for the production of anti-dsDNA. We concluded that NK T cells are involved in the progression of lupus-like disease in mature NZB/W mice and that immunoglobulin of the IgG2a isotype has an enhancing effect on antibody synthesis due to the induction of BAFF/BLyS, and therefore have a deleterious effect in the NZB/W mouse physiology.
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spelling Postol, EdilbertoMeyer, AndreCardillo, FabiolaAlencar, Raquel dePessina, DanielNihei, JorgeMariano, Mario [UNIFESP]Mengel, JoseFiocruz MSUniversidade de São Paulo (USP)Universidade Federal de São Paulo (UNIFESP)2016-01-24T13:51:42Z2016-01-24T13:51:42Z2008-10-01Immunology. Malden: Wiley-Blackwell, v. 125, n. 2, p. 184-196, 2008.0019-2805http://repositorio.unifesp.br/handle/11600/30917http://dx.doi.org/10.1111/j.1365-2567.2008.02835.x10.1111/j.1365-2567.2008.02835.xWOS:000258972400006The role of natural killer (NK) T cells in the development of lupus-like disease in mice is still controversial. We treated NZB/W mice with anti-NK1.1 monoclonal antibodies (mAbs) and our results revealed that administration of either an irrelevant immunoglobulin G2a (IgG2a) mAb or an IgG2a anti-NK1.1 mAb increased the production of anti-dsDNA antibodies in young NZB/W mice. However, the continuous administration of an anti-NK1.1 mAb protected aged NZB/W mice from glomerular injury, leading to prolonged survival and stabilization of the proteinuria. Conversely, the administration of the control IgG2a mAb led to an aggravation of the lupus-like disease. Augmented titres of anti-dsDNA in NZB/W mice, upon IgG2a administration, correlated with the production of BAFF/BLyS by dendritic, B and T cells. Treatment with an anti-NK1.1 mAb reduced the levels of interleukin-16, produced by T cells, in spleen cell culture supernatants from aged NZB/W. Adoptive transfer of NK T cells from aged to young NZB/W accelerated the production of anti-dsDNA in recipient NZB/W mice, suggesting that NK T cells from aged NZB/W are endowed with a B-cell helper activity. in vitro studies, using purified NK T cells from aged NZB/W, showed that these cells provided helper B-cell activity for the production of anti-dsDNA. We concluded that NK T cells are involved in the progression of lupus-like disease in mature NZB/W mice and that immunoglobulin of the IgG2a isotype has an enhancing effect on antibody synthesis due to the induction of BAFF/BLyS, and therefore have a deleterious effect in the NZB/W mouse physiology.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fiocruz MS, Oswaldo Cruz Fdn, IGM, BR-40296710 Salvador, BA, BrazilUniv São Paulo, Inst Heart INCOR, Immunol Lab, São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Immunol, Dept Microbiol Immunol & Parasitol, São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Immunol, Dept Microbiol Immunol & Parasitol, São Paulo, BrazilCNPq: 305835/2003-3FAPESP: 95/9379-2FAPESP: 97/06225-0Web of Science184-196engWiley-BlackwellImmunologyhttp://olabout.wiley.com/WileyCDA/Section/id-406071.htmlinfo:eu-repo/semantics/openAccessBAFF/BLySFc receptorinterleukin-16natural killer T cellssystemic lupus erythematosusToll-like receptorLong-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS productioninfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlereponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/309172022-06-02 09:27:23.803metadata only accessoai:repositorio.unifesp.br:11600/30917Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:15:38.649750Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
title Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
spellingShingle Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
Postol, Edilberto
BAFF/BLyS
Fc receptor
interleukin-16
natural killer T cells
systemic lupus erythematosus
Toll-like receptor
title_short Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
title_full Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
title_fullStr Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
title_full_unstemmed Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
title_sort Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production
author Postol, Edilberto
author_facet Postol, Edilberto
Meyer, Andre
Cardillo, Fabiola
Alencar, Raquel de
Pessina, Daniel
Nihei, Jorge
Mariano, Mario [UNIFESP]
Mengel, Jose
author_role author
author2 Meyer, Andre
Cardillo, Fabiola
Alencar, Raquel de
Pessina, Daniel
Nihei, Jorge
Mariano, Mario [UNIFESP]
Mengel, Jose
author2_role author
author
author
author
author
author
author
dc.contributor.institution.none.fl_str_mv Fiocruz MS
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Postol, Edilberto
Meyer, Andre
Cardillo, Fabiola
Alencar, Raquel de
Pessina, Daniel
Nihei, Jorge
Mariano, Mario [UNIFESP]
Mengel, Jose
dc.subject.eng.fl_str_mv BAFF/BLyS
Fc receptor
interleukin-16
natural killer T cells
systemic lupus erythematosus
Toll-like receptor
topic BAFF/BLyS
Fc receptor
interleukin-16
natural killer T cells
systemic lupus erythematosus
Toll-like receptor
description The role of natural killer (NK) T cells in the development of lupus-like disease in mice is still controversial. We treated NZB/W mice with anti-NK1.1 monoclonal antibodies (mAbs) and our results revealed that administration of either an irrelevant immunoglobulin G2a (IgG2a) mAb or an IgG2a anti-NK1.1 mAb increased the production of anti-dsDNA antibodies in young NZB/W mice. However, the continuous administration of an anti-NK1.1 mAb protected aged NZB/W mice from glomerular injury, leading to prolonged survival and stabilization of the proteinuria. Conversely, the administration of the control IgG2a mAb led to an aggravation of the lupus-like disease. Augmented titres of anti-dsDNA in NZB/W mice, upon IgG2a administration, correlated with the production of BAFF/BLyS by dendritic, B and T cells. Treatment with an anti-NK1.1 mAb reduced the levels of interleukin-16, produced by T cells, in spleen cell culture supernatants from aged NZB/W. Adoptive transfer of NK T cells from aged to young NZB/W accelerated the production of anti-dsDNA in recipient NZB/W mice, suggesting that NK T cells from aged NZB/W are endowed with a B-cell helper activity. in vitro studies, using purified NK T cells from aged NZB/W, showed that these cells provided helper B-cell activity for the production of anti-dsDNA. We concluded that NK T cells are involved in the progression of lupus-like disease in mature NZB/W mice and that immunoglobulin of the IgG2a isotype has an enhancing effect on antibody synthesis due to the induction of BAFF/BLyS, and therefore have a deleterious effect in the NZB/W mouse physiology.
publishDate 2008
dc.date.issued.fl_str_mv 2008-10-01
dc.date.accessioned.fl_str_mv 2016-01-24T13:51:42Z
dc.date.available.fl_str_mv 2016-01-24T13:51:42Z
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 Immunology. Malden: Wiley-Blackwell, v. 125, n. 2, p. 184-196, 2008.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/30917
http://dx.doi.org/10.1111/j.1365-2567.2008.02835.x
dc.identifier.issn.none.fl_str_mv 0019-2805
dc.identifier.doi.none.fl_str_mv 10.1111/j.1365-2567.2008.02835.x
dc.identifier.wos.none.fl_str_mv WOS:000258972400006
identifier_str_mv Immunology. Malden: Wiley-Blackwell, v. 125, n. 2, p. 184-196, 2008.
0019-2805
10.1111/j.1365-2567.2008.02835.x
WOS:000258972400006
url http://repositorio.unifesp.br/handle/11600/30917
http://dx.doi.org/10.1111/j.1365-2567.2008.02835.x
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv Immunology
dc.rights.driver.fl_str_mv http://olabout.wiley.com/WileyCDA/Section/id-406071.html
info:eu-repo/semantics/openAccess
rights_invalid_str_mv http://olabout.wiley.com/WileyCDA/Section/id-406071.html
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 184-196
dc.publisher.none.fl_str_mv Wiley-Blackwell
publisher.none.fl_str_mv Wiley-Blackwell
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
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