Evidence map›Paper›PMID 27328989›Full record

ArticleMucosal immunology2017

Cytokine regulation of lung Th17 response to airway immunization using LPS adjuvant.

S M Caucheteux, J Hu-Li, R N Mohammed, A Ager, W E Paul

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2017. 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
5.5field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Transcriptomic Analysis on Responses of Murine Lungs toFrontiers in cellular and infection microbiology · 2017
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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

5 authors at 2 institutions in 2 countries.

S M CaucheteuxLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
J Hu-LiLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
R N MohammedInstitute of Infection and Immunity, Cardiff University, Cardiff, UK.
A AgerInstitute of Infection and Immunity, Cardiff University, Cardiff, UK.
W E PaulLaboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USCardiff University · GB

Funding

Interleukin 4ZIAAI000493 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GERMAIN, RONALD N · 2009 to 2017
$11.5M
Lymphocyte DynamicsZIAAI000926 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI GERMAIN, RONALD N · 2009 to 2017
$9.7M
Lymphocyte DynamicsZ01AI000926 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI PAUL, WILLIAM E. · 2003 to 2008
$3.3M
Intramural NIH HHS Z01 AI000926
6 · The paper itself

Abstract

Infections caused by bacteria in the airway preferentially induce a Th17 response. However, the mechanisms involved in the regulation of CD4 T-cell responses in the lungs are incompletely understood. Here, we have investigated the mechanisms involved in the regulation of Th17 differentiation in the lungs in response to immunization with lipopolysaccharide (LPS) as an adjuvant. Our data show that both Myd88 and TRIF are necessary for Th17 induction. This distinctive fate determination can be accounted for by the pattern of inflammatory cytokines induced by airway administration of LPS. We identified the production of interleukin (IL)-1β and IL-6 by small macrophages and IL-23 by alveolar dendritic cells (DCs), favoring Th17 responses, and IL-10 repressing interferon (IFN)-γ production. Furthermore, we show that exogenous IL-1β can drastically alter Th1 responses driven by influenza and lymphocytic choriomeningitis virus infection models and induce IL-17 production. Thus, the precision of the lung immune responses to potential threats is orchestrated by the cytokine microenvironment, can be repolarized and targeted therapeutically by altering the cytokine milieu. These results indicate that how the development of Th17 responses in the lung is regulated by the cytokines produced by lung DCs and macrophages in response to intranasal immunization with LPS adjuvant.

Indexed as

Adaptor Proteins, Vesicular TransportAdministration, IntranasalAnimalsCell DifferentiationCells, CulturedCellular MicroenvironmentCytokinesImmunizationInfluenza A Virus, H1N1 SubtypeLipopolysaccharidesLungLymphocyte ActivationLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, Inbred C57BLAdaptor Proteins, Vesicular TransportCytokinesLipopolysaccharidesMyeloid Differentiation Factor 88Ticam1 protein, mouse

Identifiers

PMID27328989
PMCPMC5179326
OpenAlexW2474658120

What OpenQuestion holds

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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.