Evidence map›Paper›PMID 33159073›Full record

ArticleNature communications2020

Dermal IRF4+ dendritic cells and monocytes license CD4+ T helper cells to distinct cytokine profiles.

Kerry L Hilligan, Shiau-Choot Tang, Evelyn J Hyde, Elsa Roussel, Johannes U Mayer, Jianping Yang, Kirsty A Wakelin, Alfonso J Schmidt, Lisa M Connor, Alan Sher and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

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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

12 authors at 3 institutions in 3 countries.

Kerry L HilliganMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.ORCID 0000-0003-1238-1552
Shiau-Choot TangMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.
Evelyn J HydeMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.
Elsa RousselMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.ORCID 0000-0003-0158-2105
Johannes U MayerMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.ORCID 0000-0001-6225-7803
Jianping YangMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.
Kirsty A WakelinMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.
Alfonso J SchmidtMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.
Lisa M ConnorMalaghan Institute of Medical Research, Wellington, 6012, New Zealand.
Alan SherImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, 20892, MD, USA.ORCID 0000-0001-7053-2895
Andrew S MacDonaldLydia Becker Institute of Immunology and Inflammation, Manchester Collaborative Centre for Inflammation Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.ORCID 0000-0002-5356-1149
Franca RoncheseMalaghan Institute of Medical Research, Wellington, 6012, New Zealand. fronchese@malaghan.org.nz.ORCID 0000-0001-5835-8230
Malaghan Institute of Medical Research · NZNational Institutes of Health · USManchester Academic Health Science Centre · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council
6 · The paper itself

Abstract

Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in determining Th differentiation in pathogen-specific settings. Here, we use skin-relevant, fluorescently-labeled bacterial, helminth or fungal pathogens to track and characterize the APC populations that drive Th responses in vivo. All pathogens are taken up by a population of IRF4+ dermal migratory dendritic cells (migDC2) that similarly upregulate surface co-stimulatory molecules but express pathogen-specific cytokine and chemokine transcripts. Depletion of migDC2 reduces the amount of Ag in lymph node and the development of IFNγ, IL-4 and IL-17A responses without gain of other cytokine responses. Ag+ monocytes are an essential source of IL-12 for both innate and adaptive IFNγ production, and inhibit follicular Th cell development. Our results thus suggest that Th cell differentiation does not require specialized APC subsets, but is driven by inducible and pathogen-specific transcriptional programs in Ag+ migDC2 and monocytes.

Indexed as

AnimalsAntigen-Presenting CellsCell DifferentiationDendritic CellsFemaleInterferon-gammaInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-17Interleukin-4Lymphocyte ActivationMaleMiceMice, Inbred C57BLMonocytesSkinInterferon-gammaInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-17Interleukin-4

Identifiers

PMID33159073
PMCPMC7647995
OpenAlexW3095121751

What OpenQuestion holds

Textmetadata
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.