dc.creator | Postól, Edilberto | |
dc.creator | Meyer, André Villanova | |
dc.creator | Cardillo, Fabíola | |
dc.creator | Alencar, Raquel de | |
dc.creator | Pessina, Daniel Huber | |
dc.creator | Nihei, Jorge Sadao | |
dc.creator | Mariano, Mário | |
dc.creator | Mengele Junior, José Orivaldo | |
dc.date | 2015-06-18T17:21:29Z | |
dc.date | 2015-06-18T17:21:29Z | |
dc.date | 2008 | |
dc.date.accessioned | 2023-09-26T23:06:17Z | |
dc.date.available | 2023-09-26T23:06:17Z | |
dc.identifier | POSTÓL, E. et al. 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. Immunology, v. 125, n. 2, p. 184-196, 2008. | |
dc.identifier | 1365-2567 | |
dc.identifier | https://www.arca.fiocruz.br/handle/icict/10918 | |
dc.identifier | 10.1111/j.1365-2567.2008.02835.x | |
dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/8886884 | |
dc.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 antidsDNA
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. | |
dc.format | application/pdf | |
dc.language | eng | |
dc.publisher | Wiley | |
dc.rights | open access | |
dc.subject | BAFF/BLyS | |
dc.subject | Fc receptor | |
dc.subject | Interleukin-16 | |
dc.subject | Natural killer T cells | |
dc.subject | Systemic lupus erythematosus | |
dc.subject | Toll-like recepto | |
dc.subject | Anticorpos Monoclonais/uso terapêutico | |
dc.subject | Fator Ativador de Células B/biossíntese | |
dc.subject | Imunoglobulina G/uso terapêutico | |
dc.subject | Nefrite Lúpica/prevenção & controle | |
dc.subject | Envelhecimento/imunologia | |
dc.subject | Animais | |
dc.subject | Anticorpos Antinucleares/biossíntese | |
dc.subject | Anticorpos Monoclonais/imunologia | |
dc.subject | Antígenos Ly/imunologia | |
dc.subject | Células Cultivadas | |
dc.subject | Progressão da Doença | |
dc.subject | Feminino | |
dc.subject | Imunoglobulina G/imunologia | |
dc.subject | Interleucina-16/biossíntese | |
dc.subject | Células Matadoras Naturais/imunologia | |
dc.subject | Lipopolissacarídeos/imunologia | |
dc.subject | Fígado/imunologia | |
dc.subject | Nefrite Lúpica/imunologia | |
dc.subject | Camundongos | |
dc.subject | Subfamília B de Receptores Semelhantes a Lectina de Células | |
dc.subject | Índice de Gravidade de Doença | |
dc.subject | Linfócitos T Auxiliares-Indutores/imunologia | |
dc.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. | |
dc.type | Article | |