| Campo DC | Valor | Idioma |
|---|
| dc.contributor.author | Barroso, Daniel Holanda | - |
| dc.contributor.author | Falcão, Sarah de Athayde Couto | - |
| dc.contributor.author | Motta, Jorgeth de Oliveira Carneiro da | - |
| dc.contributor.author | Santos, Laís Sevilha dos | - |
| dc.contributor.author | Takano, Gustavo Henrique Soares | - |
| dc.contributor.author | Gomes, Ciro Martins | - |
| dc.contributor.author | Favali, Cecília Beatriz Fiuza | - |
| dc.contributor.author | Lima, Beatriz Dolabela de | - |
| dc.contributor.author | Sampaio, Raimunda Nonata Ribeiro | - |
| dc.date.accessioned | 2019-02-12T11:20:59Z | - |
| dc.date.available | 2019-02-12T11:20:59Z | - |
| dc.date.issued | 2018-05-11 | - |
| dc.identifier.citation | BARROSO, Daniel Holanda et al. PD-L1 may mediate T-cell exhaustion in a case of early diffuse Leishmaniasis caused by Leishmania (L.) amazonensis. Frontiers in Immunology, v. 9, article 1021, May 2018. DOI: https://doi.org/10.3389/fimmu.2018.01021. Disponível em: https://www.frontiersin.org/articles/10.3389/fimmu.2018.01021/full. Acesso em: 12 fev. 2019. | pt_BR |
| dc.identifier.uri | http://repositorio.unb.br/handle/10482/33985 | - |
| dc.language.iso | Inglês | pt_BR |
| dc.publisher | Frontiers | pt_BR |
| dc.rights | Acesso Aberto | pt_BR |
| dc.title | PD-L1 may mediate T-cell exhaustion in a case of early diffuse Leishmaniasis caused by Leishmania (L.) amazonensis | pt_BR |
| dc.type | Artigo | pt_BR |
| dc.subject.keyword | Leishmaniose tegumentar | pt_BR |
| dc.subject.keyword | Leishmania (Leishmania) amazonensis | pt_BR |
| dc.subject.keyword | Células | pt_BR |
| dc.subject.keyword | Enzimas | pt_BR |
| dc.subject.keyword | Citometria | pt_BR |
| dc.rights.license | Copyright © 2018 Barroso, Falcão, Motta, Sevilha-Santos, Takano, Gomes, Favali, de Lima and Sampaio. 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) and the copyright owner 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. | pt_BR |
| dc.identifier.doi | https://doi.org/10.3389/fimmu.2018.01021 | pt_BR |
| dc.description.abstract1 | Introduction: Diffuse cutaneous leishmaniasis (DCL) is a rare disease form associated
with Leishmania (L.) amazonensis in South America. It represents the “anergic” pole of
American Tegumentary Leishmaniasis, and the explanation for its resistance to treatment
remains elusive. We aimed to study some possible immunological mechanisms involved
in the poor DCL treatment response by evaluating some cell surface molecules obtained
from a patient with DCL by flow cytometry.
Case presentation: A 65-year-old DCL patient who initially failed to respond to the standard
treatment for the disease showed vacuolated macrophages filled with amastigotes in
lesion biopsy, and L. (L.) amazonensis was identified through ITS1PCR amplification. The
Leishmania skin test and indirect immunofluorescence analysis revealed negative results.
Peripheral blood from the patient was collected after a few months of treatment, when
the patient presented with no lesion. Peripheral blood mononuclear cells were analyzed
ex vivo and in vitro after 48 h of stimulation with soluble L. (L.) amazonensis antigen (SLA).
Cell death, surface molecules, and intracellular molecules, such as IFN-γ and granzyme B,
were analyzed in the cells using flow cytometry. Analysis of the surface markers showed
an increased expression of the inhibitory molecule programmed death ligand 1 (PD-L1)
in the monocytes restimulated with SLA (approximately 65%), whereas the negative
controls were 35% positive for PD-L1. Conversely, compared with the negative controls,
we observed a decrease in CD4+IFN-γ+ T cells (8.32 versus 1.7%) and CD8+IFN-γ+ T cells
(14% versus 1%). We also observed a relevant decrease in the granzyme B levels in the
CD8+ T cells, from 31% in the negative controls to 5% after SLA restimulation.
Conclusion: The dysfunctional activation of PD-L1 inhibitory pathway after Leishmania
antigen stimulation and reduced levels of IFN-gamma and granzyme B-producing cells
could be closely related to unresponssiveness to standard drug treatment of DCL patient. | pt_BR |
| dc.description.unidade | Faculdade de Medicina (FMD) | - |
| Aparece nas coleções: | Artigos publicados em periódicos e afins
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