Evidence map›Paper›PMID 23555256›Full record

ArticlePLoS pathogens2013

IL-17 mediates immunopathology in the absence of IL-10 following Leishmania major infection.

Claudia Gonzalez-Lombana, Ciara Gimblet, Olivia Bacellar, Walker W Oliveira, Sara Passos, Lucas P Carvalho, Michael Goldschmidt, Edgar M Carvalho, Phillip Scott

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
18.3field-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

88 citing papers in PubMed, 163 citations in OpenAlex.

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28 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Claudia Gonzalez-LombanaDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Ciara Gimblet
Olivia Bacellar
Walker W Oliveira
Sara Passos
Lucas P Carvalho
Michael Goldschmidt
Edgar M Carvalho
Phillip Scott
Instituto Nacional de Ciência e Tecnologia de Doenças Tropicais · BRUniversity of Pennsylvania · USUniversidade Federal da Bahia · BR

Funding

The role of Leishmania braziliensis strain polymorphism on disease outcome and ..P50AI030639 · NIAID · FEDERAL UNIVERSITY OF BAHIA · PI CARVALHO, EDGAR M · 1991 to 2023
$9.1M
PARASITOLOGY: MODERN APPROACHEST32AI007532 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HERBERT, DE'BROSKI R · 1998 to 2022
$5.0M
Initiation of Immune Response in Chronic LeishmaniasisR01AI076257 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SCOTT, PHILLIP · 2009 to 2013
$1.8M
NIAID NIH HHS AI30639NIAID NIH HHS P50 AI030639NIAID NIH HHS R01 AI-076257NIAID NIH HHS R01 AI076257NIAID NIH HHS T32 AI007532
6 · The paper itself

Abstract

Leishmaniasis, resulting from infection with the protozoan parasite Leishmania, consists of a wide spectrum of clinical manifestations, from healing cutaneous lesions to fatal visceral infections. A particularly severe form of cutaneous leishmaniasis, termed mucosal leishmaniasis, exhibits decreased IL-10 levels and an exaggerated inflammatory response that perpetuates the disease. Using a mouse model of leishmaniasis, we investigated what cytokines contribute to increased pathology when IL-10-mediated regulation is absent. Leishmania major infected C57BL/6 mice lacking IL-10 regulation developed larger lesions than controls, but fewer parasites. Both IFN-γ and IL-17 levels were substantially elevated in mice lacking the capacity to respond to IL-10. IFN-γ promoted an increased infiltration of monocytes, while IL-17 contributed to an increase in neutrophils. Surprisingly, however, we found that IFN-γ did not contribute to increased pathology, but instead regulated the IL-17 response. Thus, blocking IFN-γ led to a significant increase in IL-17, neutrophils and disease. Similarly, the production of IL-17 by cells from leishmaniasis patients was also regulated by IL-10 and IFN-γ. Additional studies found that the IL-1 receptor was required for both the IL-17 response and increased pathology. Therefore, we propose that regulating IL-17, possibly by downregulating IL-1β, may be a useful approach for controlling immunopathology in leishmaniasis.

Indexed as

AnimalsDisease Models, AnimalDown-RegulationFemaleHumansInterferon-gammaInterleukin-10Interleukin-17Interleukin-1betaLeishmania majorLeishmaniasis, CutaneousMiceMice, Inbred C57BLMice, KnockoutMonocytesNeutrophil InfiltrationInterferon-gammaInterleukin-10Interleukin-17Interleukin-1beta

Identifiers

PMID23555256
PMCPMC3605236
OpenAlexW1997570781

What OpenQuestion holds

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LicenceCC BY
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.