Evidence map›Paper›PMID 27183598›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Myeloid-Restricted AMPKα1 Promotes Host Immunity and Protects against IL-12/23p40-Dependent Lung Injury during Hookworm Infection.

Wildaliz Nieves, Li-Yin Hung, Taylor K Oniskey, Louis Boon, Marc Foretz, Benoit Viollet, De'Broski R Herbert

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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  13. AMP-Activated Protein Kinase and Host Defense against Infection.International journal of molecular sciences · 2018
    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

7 authors at 3 institutions in 3 countries.

Wildaliz NievesDivision of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA 94110;ORCID 0000-0001-9687-8333
Li-Yin HungDivision of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA 94110;
Taylor K OniskeyDivision of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA 94110;
Louis BoonEPIRUS Biopharmaceuticals Netherlands BV, 3584 CM Utrecht, the Netherlands;
Marc ForetzInstitut National de la Santé et de la Recherché Médicale U1016, Institut Cochin, 75014 Paris, France; CNRS, UMR 8104, 75014 Paris, France; and Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France.
Benoit ViolletInstitut National de la Santé et de la Recherché Médicale U1016, Institut Cochin, 75014 Paris, France; CNRS, UMR 8104, 75014 Paris, France; and Université Paris Descartes, Sorbonne Paris Cité, 75006 Paris, France.ORCID 0000-0002-0121-0224
De'Broski R HerbertDivision of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA 94110; debroski@vet.upenn.edu.ORCID 0000-0002-2449-5365
University of California, San Francisco · USDélégation Paris 5 · FRBristol-Myers Squibb (Netherlands) · NL

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
Alternative Macrophage Activation Limits ImmunopathologyR01GM083204 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI HERBERT, DE'BROSKI R · 2007 to 2018
$2.5M
Trefoil Factors Regulate Th2 ImmunityR01AI095289 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HERBERT, DE'BROSKI R · 2011 to 2015
$2.1M
NIAID NIH HHS P30 AI027763NIAID NIH HHS R01 AI095289NIAID NIH HHS T32 AI007334NIGMS NIH HHS R01 GM083204Wellcome Trust
6 · The paper itself

Abstract

How the metabolic demand of parasitism affects immune-mediated resistance is poorly understood. Immunity against parasitic helminths requires M2 cells and IL-13, secreted by CD4(+) Th2 and group 2 innate lymphoid cells (ILC2), but whether certain metabolic enzymes control disease outcome has not been addressed. This study demonstrates that AMP-activated protein kinase (AMPK), a key driver of cellular energy, regulates type 2 immunity and restricts lung injury following hookworm infection. Mice with a selective deficiency in the AMPK catalytic α1 subunit in alveolar macrophages and conventional dendritic cells produced less IL-13 and CCL17 and had impaired expansion of ILC2 in damaged lung tissue compared with wild-type controls. Defective type 2 responses were marked by increased intestinal worm burdens, exacerbated lung injury, and increased production of IL-12/23p40, which, when neutralized, restored IL-13 production and improved lung recovery. Taken together, these data indicate that defective AMPK activity in myeloid cells negatively impacts type 2 responses through increased IL-12/23p40 production. These data support an emerging concept that myeloid cells and ILC2 can coordinately regulate tissue damage at mucosal sites through mechanisms dependent on metabolic enzyme function.

Indexed as

AMP-Activated Protein KinasesAnimalsHookworm InfectionsImmunity, InnateInterleukin-12Interleukin-23Lung InjuryMiceMice, Inbred C57BLMyeloid CellsAMP-Activated Protein KinasesInterleukin-12Interleukin-23Prkaa1 protein, mouse

Identifiers

PMID27183598
PMCPMC4875814
OpenAlexW2339096411

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.