Evidence map›Paper›PMID 26104914›Full record

ArticleMucosal immunology2016

Antigen-specific cytotoxic T lymphocytes target airway CD103+ and CD11b+ dendritic cells to suppress allergic inflammation.

N J Daniels, E Hyde, S Ghosh, K Seo, K M Price, K Hoshino, T Kaisho, T Okada, F Ronchese

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In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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  10. In vivo multiphoton imaging of immune cell dynamics.Pflugers Archiv : European journal of physiology · 2016
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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

9 authors at 5 institutions in 2 countries.

N J DanielsMalaghan Institute of Medical Research, Wellington, New Zealand.
E HydeMalaghan Institute of Medical Research, Wellington, New Zealand.
S GhoshMalaghan Institute of Medical Research, Wellington, New Zealand.
K SeoLab for Tissue Dynamics, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Japan.
K M PriceMalaghan Institute of Medical Research, Wellington, New Zealand.
K HoshinoLaboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Japan.
T KaishoLaboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Japan.
T OkadaLab for Tissue Dynamics, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Japan.
F RoncheseMalaghan Institute of Medical Research, Wellington, New Zealand.
Malaghan Institute of Medical Research · NZJapan Science and Technology Agency · JPKagawa University · JPRIKEN Center for Integrative Medical Sciences · JPWakayama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic airway inflammation is driven by the recognition of inhaled allergen by T helper type 2 (Th2) cells in the airway and lung. Allergen-specific cytotoxic T lymphocytes (CTLs) can strongly reduce airway inflammation, however, the mechanism of their inhibitory activity is not fully defined. We used mouse models to show that allergen-specific CTLs reduced early cytokine production by Th2 cells in lung, and their subsequent accumulation and production of interleukin (IL)-4 and IL-13. In addition, treatment with specific CTLs also increased the proportion of caspase(+) dendritic cells (DCs) in mediastinal lymph node (MLN), and decreased the numbers of CD103(+) and CD11b(+) DCs in the lung. This decrease required expression of the cytotoxic mediator perforin in CTLs and of the appropriate MHC-antigen ligand on DCs, suggesting that direct CTL-DC contact was necessary. Lastly, lung imaging experiments revealed that in airway-challenged mice XCR1-GFP(+) DCs, corresponding to the CD103(+) DC subset, and XCR1-GFP(-) CD11c(+) cells, which include CD11b(+) DCs and alveolar macrophages, both clustered in the areas surrounding the small airways and were closely associated with allergen-specific CTLs. Thus, allergen-specific CTLs reduce allergic airway inflammation by depleting CD103(+) and CD11b(+) DC populations in the lung, and may constitute a mechanism through which allergic immune responses are regulated.

Indexed as

AnimalsAntigens, CDCaspasesCD11b AntigenCell DeathDendritic CellsFemaleGene Expression RegulationGenes, ReporterGreen Fluorescent ProteinsIntegrin alpha ChainsInterleukin-13Interleukin-4LungMaleMicealpha E integrinsAntigens, CDCaspasesCD11b AntigenGreen Fluorescent ProteinsIntegrin alpha ChainsInterleukin-13Interleukin-4Ovalbuminperforin, mousePore Forming Cytotoxic ProteinsReceptors, G-Protein-CoupledXCR1 protein, human

Identifiers

PMID26104914
OpenAlexW812216563

What OpenQuestion holds

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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.