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dc.contributor.authorFerreira, Camila Pontes
dc.contributor.authorCariste, Leonardo Moro.
dc.contributor.authorSantos Virgilio, Fernando Dos.
dc.contributor.authorMoraschi, Barbara Ferri
dc.contributor.authorMonteiro, Caroline Brandao.
dc.contributor.authorVieira Machado, Alexandre M.
dc.contributor.authorGazzinelli, Ricardo T.
dc.contributor.authorBruna-Romero, Oscar
dc.contributor.authorMenin Ruiz, Pedro Luiz.
dc.contributor.authorRibeiro, Daniel Araki
dc.contributor.authorLannes-Vieira, Joseli
dc.contributor.authorLopes, Marcela de Freitas
dc.contributor.authorRodrigues, Mauricio Martins
dc.contributor.authorde Vasconcelos, Jose Ronnie. Carvalho
dc.date2022-08-11T08:09:49.000
dc.date.accessioned2022-08-23T16:44:22Z
dc.date.available2022-08-23T16:44:22Z
dc.date.issued2017-10-13
dc.date.submitted2018-03-14
dc.identifier.citation<p>Front Immunol. 2017 Oct 13;8:1291. doi: 10.3389/fimmu.2017.01291. eCollection 2017. <a href="https://doi.org/10.3389/fimmu.2017.01291">Link to article on publisher's site</a></p>
dc.identifier.issn1664-3224 (Linking)
dc.identifier.doi10.3389/fimmu.2017.01291
dc.identifier.pmid29081775
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40488
dc.description.abstractIntegrins 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.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29081775&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright: © 2017 Ferreira, Cariste, Santos Virgílio, Moraschi, Monteiro, Vieira Machado, Gazzinelli, Bruna-Romero, Menin Ruiz, Ribeiro, Lannes-Vieira, Lopes, Rodrigues and Vasconcelos. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectTrypanosoma cruzi
dc.subjectintegrins
dc.subjectmigration
dc.subjectspecific CD8+ T cells
dc.subjectvaccination
dc.subjectImmunology of Infectious Disease
dc.subjectImmunoprophylaxis and Therapy
dc.subjectInfectious Disease
dc.subjectParasitic Diseases
dc.subjectParasitology
dc.titleLFA-1 Mediates Cytotoxicity and Tissue Migration of Specific CD8(+) T Cells after Heterologous Prime-Boost Vaccination against Trypanosoma cruzi Infection
dc.typeJournal Article
dc.source.journaltitleFrontiers in immunology
dc.source.volume8
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4304&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3293
dc.identifier.contextkey11771536
refterms.dateFOA2022-08-23T16:44:23Z
html.description.abstract<p>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.</p>
dc.identifier.submissionpathoapubs/3293
dc.contributor.departmentDivision of Infectious Disease and Immunology, Department of Medicine
dc.source.pages1291


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Copyright: © 2017 Ferreira, Cariste, Santos Virgílio, Moraschi, Monteiro, Vieira Machado, Gazzinelli, Bruna-Romero, Menin Ruiz, Ribeiro, Lannes-Vieira, Lopes, Rodrigues and Vasconcelos. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Except where otherwise noted, this item's license is described as Copyright: © 2017 Ferreira, Cariste, Santos Virgílio, Moraschi, Monteiro, Vieira Machado, Gazzinelli, Bruna-Romero, Menin Ruiz, Ribeiro, Lannes-Vieira, Lopes, Rodrigues and Vasconcelos. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.