Evidence map›Paper›PMID 30845223›Full record

ArticlePLoS neglected tropical diseases2019

Host and parasite responses in human diffuse cutaneous leishmaniasis caused by L. amazonensis.

Stephen M Christensen, Ashton T Belew, Najib M El-Sayed, Wagner L Tafuri, Fernando T Silveira, David M Mosser

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

45 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Leishmaniasis.Nature reviews. Disease primers · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Identification of driving genes of familial adenomatous polyposis by differential gene expression analysis and weighted gene co-expression network analysis.Technology and health care : official journal of the European Society for Engineering and Medicine · 2024
    Article
  18. Article
  19. 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

6 authors at 3 institutions in 2 countries.

Stephen M ChristensenDepartment of Cell Biology and Molecular Genetics and the Maryland Pathogen Research Institute, University of Maryland, College Park, MD United States of America.ORCID 0000-0002-3618-6420
Ashton T BelewDepartment of Cell Biology and Molecular Genetics and the Maryland Pathogen Research Institute, University of Maryland, College Park, MD United States of America.
Najib M El-SayedDepartment of Cell Biology and Molecular Genetics and the Maryland Pathogen Research Institute, University of Maryland, College Park, MD United States of America.
Wagner L TafuriDepartamento de Patologia Geral, Universidade Federal de Minas Geras, Belo Horizonte, Brazil.
Fernando T SilveiraEvandro Chagas Institute, Tropical Medicine Nucleus, Federal University of Pará, Belém, PA Brazil.
David M MosserDepartment of Cell Biology and Molecular Genetics and the Maryland Pathogen Research Institute, University of Maryland, College Park, MD United States of America.
University of Maryland, College Park · USUniversidade Federal de Minas Gerais · BRUniversidade Federal do Pará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diffuse cutaneous leishmaniasis (DCL) is a rare form of leishmaniasis where parasites grow uncontrolled in diffuse lesions across the skin. Meta-transcriptomic analysis of biopsies from DCL patients infected with Leishmania amazonensis demonstrated an infiltration of atypical B cells producing a surprising preponderance of the IgG4 isotype. DCL lesions contained minimal CD8+ T cell transcripts and no evidence of persistent TH2 responses. Whereas localized disease exhibited activated (so-called M1) macrophage presence, transcripts in DCL suggested a regulatory macrophage (R-Mϕ) phenotype with higher levels of ABCB5, DCSTAMP, SPP1, SLAMF9, PPARG, MMPs, and TM4SF19. The high levels of parasite transcripts in DCL and the remarkable uniformity among patients afforded a unique opportunity to study parasite gene expression in this disease. Patterns of parasite gene expression in DCL more closely resembled in vitro parasite growth in resting macrophages, in the absence of T cells. In contrast, parasite gene expression in LCL revealed 336 parasite genes that were differently upregulated, relative to DCL and in vitro macrophage growth, and these transcripts may represent transcripts that are produced by the parasite in response to host immune pressure.

Indexed as

AdolescentAdultAntigens, ProtozoanFemaleHost-Parasite InteractionsHumansImmunoglobulin GLeishmaniaLeishmaniasis, Diffuse CutaneousMacrophagesMaleMiddle AgedT-Lymphocytes, CytotoxicTranscriptomeAntigens, ProtozoanImmunoglobulin G

Identifiers

PMID30845223
PMCPMC6405045
OpenAlexW2920836773

What OpenQuestion holds

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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.