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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

LFA-1 Mediates Cytotoxicity and Tissue Migration of Specific CD8(+) T Cells after Heterologous Prime-Boost Vaccination against Trypanosoma cruzi Infection

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Author(s):
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Ferreira, Camila Pontes [1, 2] ; Cariste, Leonardo Moro [1, 3] ; Virgilio, Fernando Dos Santos [1, 2] ; Moraschi, Barbara Ferri [1, 2] ; Monteiro, Caroline Brandao [3] ; Vieira Machado, Alexandre M. [4] ; Gazzinelli, Ricardo Tostes [4, 5] ; Bruna-Romero, Oscar [6] ; Menin Ruiz, Pedro Luiz [3] ; Ribeiro, Daniel Araki [3] ; Lannes-Vieira, Joseli [7] ; Lopes, Marcela de Freitas [8] ; Rodrigues, Mauricio Martins [1, 2] ; Carvalho de Vasconcelos, Jose Ronnie [3, 1, 2]
Total Authors: 14
Affiliation:
[1] Ctr Mol & Cellular Therapy, Mol Immunol Lab, Sao Paulo - Brazil
[2] Fed Univ Sao Paulo UNIFESP, Dept Microbiol Immunol & Parasitol, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Biosci, Sao Paulo - Brazil
[4] Fiocruz MS, Rene Rachou Res Ctr, Belo Horizonte, MG - Brazil
[5] Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis & Immunol, Worcester, MA - USA
[6] Univ Fed Santa Catarina, Dept Microbiol Immunol & Parasitol, Florianopolis, SC - Brazil
[7] Fiocruz MS, Oswaldo Cruz Inst, Biol Interact Lab, Rio De Janeiro - Brazil
[8] Univ Fed Rio de Janeiro, Inst Biophys Carlos Chagas Filho, Rio De Janeiro - Brazil
Total Affiliations: 8
Document type: Journal article
Source: FRONTIERS IN IMMUNOLOGY; v. 8, OCT 13 2017.
Web of Science Citations: 3
Abstract

Integrins mediate the lymphocyte migration into an infected tissue, and these cells are essential for controlling the multiplication of many intracellular parasites such as Trypanosoma cruzi, the causative agent of Chagas disease. Here, we explore LFA-1 and VLA-4 roles in the migration of specific CD8(+) T cells generated by heterologous prime-boost immunization during experimental infection with T. cruzi. To this end, vaccinated mice were treated with monoclonal anti-LFA-1 and/or anti-VLA-4 to block these molecules. After anti-LFA-1, but not anti-VLA-4 treatment, all vaccinated mice displayed increased blood and tissue parasitemia, and quickly succumbed to infection. In addition, there was an accumulation of specific CD8(+) T cells in the spleen and lymph nodes and a decrease in the number of those cells, especially in the heart, suggesting that LFA-1 is important for the output of specific CD8(+) T cells from secondary lymphoid organs into infected organs such as the heart. The treatment did not alter CD8(+) T cell effector functions such as the production of pro-inflammatory cytokines and granzyme B, and maintained the proliferative capacity after treatment. However, the specific CD8(+) T cell direct cytotoxicity was impaired after LFA-1 blockade. Also, these cells expressed higher levels of Fas/CD95 on the surface, suggesting that they are susceptible to programmed cell death by the extrinsic pathway. We conclude that LFA-1 plays an important role in the migration of specific CD8(+) T cells and in the direct cytotoxicity of these cells. (AU)

FAPESP's process: 12/22514-3 - Migration study of specific T cells generated by vaccination or Trypanosoma cruzi infection
Grantee:Jose Ronnie Carvalho de Vasconcelos
Support type: Research Grants - Young Investigators Grants
FAPESP's process: 15/08814-2 - Role of integrin receptors and chemokines in the migration of specific CD8+ T cells generated by genetic immunization with ASP -2 Trypanosoma cruzi
Grantee:Camila Pontes Ferreira
Support type: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 14/19422-5 - Pharmacological effect of the mTOR inhibitor rapamycin in response to memory CD8+ t lymphocytes induced by genetic immunization using heterologous prime-boost
Grantee:Barbara Ferri Moraschi
Support type: Scholarships in Brazil - Master
FAPESP's process: 17/11499-7 - Role of CX3CR1 chemokine receptor and the integrin LFA-1 in the differentiation and activation of CD8 + t lymphocytes during Trypanosoma cruzi infection
Grantee:Leonardo Moro Cariste
Support type: Scholarships in Brazil - Master