Evidence map›Paper›PMID 23053396›Full record

ReviewSeminars in immunopathology2012

Immunopathogenesis of non-healing American cutaneous leishmaniasis and progressive visceral leishmaniasis.

Lynn Soong, Calvin A Henard, Peter C Melby

Open access · bronzeAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Revival of Leishmanization and Leishmanin.Frontiers in cellular and infection microbiology · 2021
    Review
  15. Review
  16. Role of Host and Parasite MIF Cytokines duringTropical medicine and infectious disease · 2020
    Review
  17. Review
  18. Molecules (Basel, Switzerland) · 2019
    Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Lynn SoongDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555-1070, USA. lysoong@utmb.edu
Calvin A Henard
Peter C Melby
The University of Texas Medical Branch at Galveston · US

Funding

PATHOGENIC MECHANISMS OF CUTANEOUS LEISHMANIASISR01AI043003 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SOONG, LYNN · 1999 to 2010
$2.3M
NOS2 and arginase in visceral leishmaniasisR01AI061624 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MELBY, PETER C. · 2005 to 2009
$1.5M
Characterization of CCR5-like Molecules in LeishmaniaR21AI076849 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SOONG, LYNN · 2008 to 2010
$565k
Pathogenic Mechanisms of Cutaneous LeishmaniasisR56AI043003 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SOONG, LYNN · 2012 to 2012
$306k
NIAID NIH HHS AI00753613NIAID NIH HHS AI043003NIAID NIH HHS AI061624NIAID NIH HHS AI076849NIAID NIH HHS R01 AI043003NIAID NIH HHS R01 AI061624NIAID NIH HHS R21 AI076849NIAID NIH HHS R56 AI043003
6 · The paper itself

Abstract

The outcomes of Leishmania infection are determined by host immune and nutrition status, parasite species, and co-infection with other pathogens. While subclinical infection and self-healing cutaneous leishmaniasis (CL) are common, uncontrolled parasite replication can lead to non-healing local lesions or visceral leishmaniasis (VL). It is known that infection control requires Th1-differentiation cytokines (IL-12, IL-18, and IL-27) and Th1 cell and macrophage activation. However, there is no generalized consensus for the mechanisms of host susceptibility. The recent studies on regulatory T cells and IL-17-producing cells help explain the effector T cell responses that occur independently of the known Th1/Th2 cell signaling pathways. This review focuses on the immunopathogenesis of non-healing American CL and progressive VL. We summarize recent evidence from human and animal studies that reveals the mechanisms of dysregulated, hyper-responses to Leishmania braziliensis, as well as the presence of disease-promoting or the absence of protective responses to Leishmania amazonensis and Leishmania donovani. We highlight immune-mediated parasite growth and immunopathogenesis, with an emphasis on the putative roles of IL-17 and its related cytokines as well as arginase. A better understanding of the quality and regulation of innate immunity and T cell responses triggered by Leishmania will aid in the rational control of pathology and the infection.

Indexed as

AnimalsCoinfectionCricetinaeCytokinesDisease Models, AnimalHumansLeishmaniaLeishmaniasis, CutaneousLeishmaniasis, VisceralMiceT-Lymphocyte SubsetsCytokines

Identifiers

PMID23053396
PMCPMC4111229
OpenAlexW1973105583

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.