Evidence map›Paper›PMID 26581600›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

IL-17A promotes susceptibility during experimental visceral leishmaniasis caused by Leishmania donovani.

Cesar Terrazas, Sanjay Varikuti, Jennifer Kimble, Ellen Moretti, Prosper N Boyaka, Abhay R Satoskar

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

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  17. Revival of Leishmanization and Leishmanin.Frontiers in cellular and infection microbiology · 2021
    Review
  18. Role of Cytokines in Experimental and Human Visceral Leishmaniasis.Frontiers in cellular and infection microbiology · 2021
    Review
  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 1 institution in 1 country.

Cesar Terrazas*Department of Pathology, Department of Veterinary Biosciences, and Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA cterrazas.05@gmail.com abhay.satoskar@osumc.edu.
Sanjay Varikuti*Department of Pathology, Department of Veterinary Biosciences, and Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA.
Jennifer Kimble*Department of Pathology, Department of Veterinary Biosciences, and Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA.
Ellen Moretti*Department of Pathology, Department of Veterinary Biosciences, and Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA.
Prosper N Boyaka*Department of Pathology, Department of Veterinary Biosciences, and Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA.
Abhay R Satoskar*Department of Pathology, Department of Veterinary Biosciences, and Department of Internal Medicine, The Ohio State University, Columbus, Ohio, USA cterrazas.05@gmail.com abhay.satoskar@osumc.edu.
The Ohio State University · US

Funding

MOLECULAR ADJUVANTS FOR NALT-BASED IMMUNITY TO ANTHRAXR01AI043197 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BOYAKA, PROSPER N · 1998 to 2013
$4.6M
Regulation of mucosal IgA and allergic inflammation by intestinal epithelial cellsR01DK101323 · NIDDK · OHIO STATE UNIVERSITY · PI BOYAKA, PROSPER N · 2015 to 2019
$1.7M
NIAID NIH HHS R01 AI043197NIDDK NIH HHS R01 DK101323
6 · The paper itself

Abstract

Leishmania donovani is an intracellular parasite that infects professional phagocytes and causes visceral leishmaniasis (VL). The immune response during VL has been extensively studied in the context of T-helper (Th)1 and Th2 responses. Immunity against this parasite is dependent on IFN-γ production and subsequent macrophage activation, and the Th2 response promotes granuloma formation. The cytokine IL-17A is associated with neutrophilic inflammation. Depletion of neutrophils during experimental VL results in enhanced parasitic loads. Furthermore, although patients resistant to VL showed enhanced levels of IL-17A in circulation, little is known about the role of IL-17A during VL infection. Here, we used IL-17A-deficient mice and IL-17A reporter mice to address the role of IL-17A during VL. IL-17A(-/-) mice were highly resistant to VL infection, showing decreased parasites in the liver and spleen. This unexpected phenotype was associated with enhanced IFN-γ production by T cells and decreased accumulation of neutrophils and monocytes, resulting in reduced number of granulomas. We also found γδ T and Th17 cells as the main IL-17A(+) cells during VL infection. Our data reveal an unexpected role of IL-17A rendering susceptibility against L. donovani by regulating the IFN-γ response and promoting detrimental inflammation.

Indexed as

AnimalsDisease SusceptibilityGranulomaInterferon-gammaInterleukin-17Leishmania donovaniLeishmaniasis, VisceralLymphocyte ActivationMiceMice, Inbred C57BLMonocytesNeutrophilsReceptors, Interleukin-17Th1 CellsTh2 CellsInterferon-gammaInterleukin-17Receptors, Interleukin-17granulomamonocytesneutrophilsTh17γδ T cells

Identifiers

PMID26581600
PMCPMC4750409
OpenAlexW2311675130

What OpenQuestion holds

Textmetadata
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.