Evidence map›Paper›PMID 26903606›Full record

ArticleThe American journal of tropical medicine and hygiene2016

Development of Type 2, But Not Type 1, Leprosy Reactions is Associated with a Severe Reduction of Circulating and In situ Regulatory T-Cells.

Ana Paula Vieira, Maria Ângela Bianconcini Trindade, Carla Pagliari, João Avancini, Neusa Yurico Sakai-Valente, Alberto José da Silva Duarte, Gil Benard

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of tropical medicine and hygiene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Ana Paula VieiraLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil.
Maria Ângela Bianconcini TrindadeLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil.
Carla PagliariLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil.
João AvanciniLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil.
Neusa Yurico Sakai-ValenteLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil.
Alberto José da Silva DuarteLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil.
Gil BenardLaboratory of Medical Investigation Unit 56, Division of Clinical Dermatology, Medical School, University of São Paulo, São Paulo, Brazil; Department of Pathology, Medical School, University of São Paulo, São Paulo, Brazil; São Paulo State Health Department, Health Institute, São Paulo, Brazil; Laboratory of Medical Investigation Unit 53, Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil mahong@usp.br.
Ministério da Saúde · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leprosy is frequently complicated by the appearance of reactions that are difficult to treat and are the main cause of sequelae. We speculated that disturbances in regulatory T-cells (Tregs) could play a role in leprosy reactions. We determined the frequency of circulating Tregs in patients with type 1 reaction (T1R) and type 2 reaction (T2R). The in situ frequency of Tregs and interleukin (IL)-17, IL-6, and transforming growth factor beta (TGF)-β-expressing cells was also determined. T2R patients showed markedly lower number of circulating and in situ Tregs than T1R patients and controls. This decrease was paralleled by increased in situ IL-17 expression but decreased TGF-β expression. Biopsies from T1R and T2R patients before the reaction episodes showed similar number of forkhead box protein P3+ (FoxP3+) and IL-17+ cells. However, in biopsies taken during the reaction, T2R patients showed a decrease in Tregs and increase in IL-17+ cells, whereas T1R patients showed the opposite: Tregs increased but IL-17+ cells decreased. We also found decreased expansion of Tregs upon in vitro stimulation with Mycobacterium leprae and a trend for lower expression of FoxP3 and the immunosuppressive molecule cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) in T2R Tregs. Our results provide some evidence to the hypothesis that, in T2R, downmodulation of Tregs may favor the development of T-helper-17 responses that characterize this reaction.

Indexed as

AdultFemaleFlow CytometryHumansImmunity, CellularInterleukin-17Interleukin-6LeprosyLymphocyte CountMaleMiddle AgedT-Lymphocytes, RegulatoryTransforming Growth Factor betaInterleukin-17Interleukin-6Transforming Growth Factor beta

Identifiers

PMID26903606
PMCPMC4824210
OpenAlexW2312415181

What OpenQuestion holds

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Registered trials

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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.