Evidence map›Paper›PMID 34325119›Full record

ArticleCytokine2021

Phenotypical characterization of regulatory T cells in acute Zika infection.

Isabel Cristina Guerra-Gomes, Bruna Macêdo Gois, Rephany Fonseca Peixoto, Pedro Henrique de Sousa Palmeira, Cínthia Nóbrega de Sousa Dias, Bárbara Guimarães Csordas, Josélio Maria Galvão Araújo, Robson Cavalcante Veras, Isac Almeida de Medeiros, Fátima de Lourdes Assunção Araújo de Azevedo and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Isabel Cristina Guerra-GomesImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Bruna Macêdo GoisImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Rephany Fonseca PeixotoImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Pedro Henrique de Sousa PalmeiraImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Cínthia Nóbrega de Sousa DiasImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Bárbara Guimarães CsordasImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Josélio Maria Galvão AraújoMolecular Biology of Cancer and Infectious Diseases Laboratory of Post-Graduation Program on Parasite Biology, Federal University of Rio Grande do Norte, Natal, Rio Grande do Norte 58078-970, Brazil.
Robson Cavalcante VerasResearch Institute for Drugs and Medicines, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Isac Almeida de MedeirosResearch Institute for Drugs and Medicines, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Fátima de Lourdes Assunção Araújo de AzevedoResearch Institute for Drugs and Medicines, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil.
Rosemary Jane BoytonDepartment of Infectious Disease, Faculty of Medicine, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, United Kingdom.
Daniel Martin AltmannDepartment of Immunology and Inflammation, Faculty of Medicine, Hammersmith Hospital Campus, Imperial College London, London W12 0NN, United Kingdom.
Tatjana Souza Lima KeesenImmunology of Infectious Diseases Laboratory of Department of Cellular and Molecular Biology, Federal University of Paraiba, João Pessoa, Paraíba 58051-900, Brazil. Electronic address: tat.keesen@cbiotec.ufpb.br.
Universidade Federal da Paraíba · BRHammersmith Hospital · GBImperial College London · GBUniversidade Federal do Rio Grande do Norte · BR

Funding

Medical Research Council MC_PC_15106NIAID NIH HHS HHSN272200900046CNIAID NIH HHS HHSN272201400049CWellcome Trust
6 · The paper itself

Abstract

Zika virus (ZIKV), alongside Dengue virus (DENV), Chikungunya virus (CHIKV), and Yellow Fever Virus (YFV) are prevalent arboviruses in the Americas. Each of these infections is associated with the development of associated disease immunopathology. Immunopathological processes are an outcome of counter-balancing impacts between effector and regulatory immune mechanisms. In this context, regulatory T cells (Tregs) are key in modulating the immune response and, therefore, in tissue damage control. However, to date, Treg phenotypes and mechanisms during acute infection of the ZIKV in humans have not been fully investigated. The main aim of this work was to characterize Tregs and their immunological profile related to cytokine production and molecules that are capable of controlling the exacerbated inflammatory profile in acute Zika infected patients. Using whole blood analyses of infected patients, an ex vivo phenotypical characterization of Tregs, circulating during acute Zika virus infection, was conducted by flow cytometry. We found that though there are no differences in absolute Treg frequency between infected and healthy control groups. However, pro-inflammatory cytokine up-regulation such as IFN-γ and LAP was observed in the acute disease. Furthermore, acute ZIKV patients expressed increased levels of CD39/CD73, perforin/granzyme B, PD-1, and CTLA-4, all markers involved in mechanisms used by Tregs to attempt to control strong inflammatory responses. Thus, the data indicates a potential contribution of Tregs during the inflammatory ZIKV infection response.

Indexed as

AdultCase-Control StudiesCell DeathCytokinesFemaleHumansMalePhenotypeT-Lymphocytes, RegulatoryZika VirusZika Virus InfectionCytokinesBloodHumanInfectionT cellsViral

Identifiers

PMID34325119
PMCPMC8405058
OpenAlexW3184951983

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.