Evidence map›Paper›PMID 25191842›Full record

ArticlePloS one2014

An in vitro model of antibody-enhanced killing of the intracellular parasite Leishmania amazonensis.

Katherine N Gibson-Corley, Marie M Bockenstedt, Huijuan Li, Paola M Boggiatto, Yashdeep Phanse, Christine A Petersen, Bryan H Bellaire, Douglas E Jones

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. The balancing act: Immunology of leishmaniosis.Research in veterinary science · 2020
    Review
  4. Kinetics of Mimivirus Infection Stages Quantified Using Image Flow Cytometry.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2019
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Characterization of the B cell response to Leishmania infection after anti-CD20 B cell depletion.International journal of clinical and experimental pathology · 2015
    Article
  13. 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

8 authors.

Katherine N Gibson-CorleyDepartment of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Marie M BockenstedtDepartment of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Huijuan LiDepartment of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Paola M BoggiattoDepartment of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Yashdeep PhanseDepartment of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Christine A PetersenDepartment of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Bryan H BellaireDepartment of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.
Douglas E JonesDepartment of Veterinary Pathology, College of Veterinary Medicine, Iowa State University, Ames, Iowa, United States of America.

Funding

Role of B cells in the Cell-Mediated Immune Response to Leishmania amazonensisK08AI076616 · NIAID · IOWA STATE UNIVERSITY · PI GIBSON-CORLEY, KATHERINE NICOLE · 2008 to 2010
$353k
NIAID NIH HHS K08 AI076616NIAID NIH HHS KO8 AI076616
6 · The paper itself

Abstract

Footpad infection of C3HeB/FeJ mice with Leishmania amazonensis leads to chronic lesions accompanied by large parasite loads. Co-infecting these animals with L. major leads to induction of an effective Th1 immune response that can resolve these lesions. This cross-protection can be recapitulated in vitro by using immune cells from L. major-infected animals to effectively activate L. amazonensis-infected macrophages to kill the parasite. We have shown previously that the B cell population and their IgG2a antibodies are required for effective cross-protection. Here we demonstrate that, in contrast to L. major, killing L. amazonensis parasites is dependent upon FcRγ common-chain and NADPH oxidase-generated superoxide from infected macrophages. Superoxide production coincided with killing of L. amazonensis at five days post-activation, suggesting that opsonization of the parasites was not a likely mechanism of the antibody response. Therefore we tested the hypothesis that non-specific immune complexes could provide a mechanism of FcRγ common-chain/NADPH oxidase dependent parasite killing. Macrophage activation in response to soluble IgG2a immune complexes, IFN-γ and parasite antigen was effective in significantly reducing the percentage of macrophages infected with L. amazonensis. These results define a host protection mechanism effective during Leishmania infection and demonstrate for the first time a novel means by which IgG antibodies can enhance killing of an intracellular pathogen.

Indexed as

AnimalsAntibodies, ProtozoanAntibody-Dependent Cell CytotoxicityAntigen-Antibody ComplexDisease Models, AnimalFemaleImmunoglobulin GIn Vitro TechniquesLeishmania mexicanaLeishmaniasis, CutaneousMacrophage ActivationMacrophagesMiceMice, KnockoutNADPH OxidasesPhosphatidylinositol 3-KinasesAntibodies, ProtozoanAntigen-Antibody ComplexImmunoglobulin GNADPH OxidasesPhosphatidylinositol 3-KinasesReceptors, IgGSuperoxides

Identifiers

PMID25191842
PMCPMC4156363

What OpenQuestion holds

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LicenceCC BY
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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.