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
Autor(a) principal: | |
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Data de Publicação: | 2008 |
Outros Autores: | , , , , , , |
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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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:34652022-06-02T12:27:23Repositório 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 |
|
_version_ |
1802764136055046144 |