Author | Silva Filho, J. L. | |
Author | Souza, M. C. | |
Author | Henriques, M. G. | |
Author | Morrot, A. | |
Author | Savino, Wilson | |
Author | Neves, C. Caruso | |
Author | Pinheiro, A. A. S. | |
Access date | 2015-11-03T13:10:04Z | |
Available date | 2016-05-01T07:30:06Z | |
Document date | 2015 | |
Citation | SILVA FILHO, J. L. et al. Renin–angiotensin system contributes to naive T-cell migration in vivo. Archives of Biochemistry and Biophysics, v.573, p.1-13, May 2015. | pt_BR |
ISSN | 0003-9861 | |
URI | https://www.arca.fiocruz.br/handle/icict/12105 | |
Language | eng | pt_BR |
Publisher | ScienceDirect | pt_BR |
Rights | open access | |
Title | Renin–angiotensin system contributes to naive T-cell migration in vivo | pt_BR |
Type | Article | |
DOI | 10.1016/j.abb.2015.02.035 | |
Abstract | Angiotensin II (Ang II) plays an important role in the regulation of the T-cell response during inflammation.
However, the cellular mechanisms underlying the regulation of lymphocytes under physiologic conditions
have not yet been studied. Here, we tested the influence of Ang II on T-cell migration using T cells
from BALB/c mice. The results obtained in vivo showed that when Ang II production or the AT1 receptor
were blocked, T-cell counts were enhanced in blood but decreased in the spleen. The significance of these
effects was confirmed by observing that these cells migrate, through fibronectin to Ang II via the AT1
receptor. We also observed a gradient of Ang II from peripheral blood to the spleen, which explains its
chemotactic effect on this organ. The following cellular mechanisms were identified to mediate the
Ang II effect: upregulation of the chemokine receptor CCR9; upregulation of the adhesion molecule
CD62L; increased production of the chemokines CCL19 and CCL25 in the spleen. These results indicate
that the higher levels of Ang II in the spleen and AT1 receptor activation contribute to migration of naive
T cells to the spleen, which expands our understanding on how the Ang II/AT1 receptor axis contributes to
adaptive immunity. | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil. | pt_BR |
Affilliation | Fundação Oswaldo Cruz. Instituto de Tecnologia em Fármacos. Rio de Janeiro, RJ, Brasil. | pt_BR |
Affilliation | Fundação Oswaldo Cruz. Instituto de Tecnologia em Fármacos. Rio de Janeiro, RJ, Brasil. | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Microbiologia Professor Paulo de Góes. Rio de Janeiro, RJ, Brasil. | pt_BR |
Affilliation | Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Imunologia. Rio de Janeiro, RJ, Brasil. | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil / Conselho Nacional de Desenvolvimento Científico e Tecnológico/MCT. Instituto Nacional de Ciência e Tecnologia em Biologia e Bioimagem. Brasil. | pt_BR |
Affilliation | Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil / Conselho Nacional de Desenvolvimento Científico e Tecnológico/MCT. Instituto Nacional para Pesquisa Translacional em Saúde e Ambiente na Região Amazônica. Brasil. | pt_BR |
Subject | Renin–angiotensin system | pt_BR |
Subject | Angiotensin receptors | pt_BR |
Subject | Adaptive immunity | pt_BR |
Subject | Lymphoid organs | pt_BR |
Subject | Chemokine | pt_BR |
DeCS | Quimiocinas | pt_BR |
DeCS | Linfóide | pt_BR |
DeCS | Sistema Renina-Angiotensina | pt_BR |
DeCS | Receptores de Angiotensina | pt_BR |
e-ISSN | 1096-0384 | |
Embargo date | 2016-04-30 | |