Evidence map›Paper›PMID 26489517›Full record

ArticleScientific reports2015

Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity.

Catharina Sagita Moniaga, Sachiko Watanabe, Tetsuya Honda, Søren Nielsen, Mariko Hara-Chikuma

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. 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
3.2field-weighted citation impact, top 8% 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, 47 citations in OpenAlex.

  1. Article
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  9. The multifaceted role of aquaporins in physiological cell migration.American journal of physiology. Cell physiology · 2023
    Review
  10. Article
  11. Aquaporins in Skin.Advances in experimental medicine and biology · 2023
    Article
  12. Aquaporins in Immune System.Advances in experimental medicine and biology · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. 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

5 authors at 3 institutions in 3 countries.

Catharina Sagita MoniagaCenter for Innovation in Immunoregulative Technology and Therapeutics.
Sachiko WatanabeCenter for Innovation in Immunoregulative Technology and Therapeutics.
Tetsuya HondaCenter for Innovation in Immunoregulative Technology and Therapeutics.
Søren NielsenDepartment of Health Science and Technology, Aalborg University, Aalborg 9220, Denmark.
Mariko Hara-ChikumaCenter for Innovation in Immunoregulative Technology and Therapeutics.
Center for Innovation · USAalborg University · DKKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aquaporin-9 (AQP9), a water/glycerol channel protein, is expressed in several immune cells including neutrophils; however, its role in immune response remains unknown. Here we show the involvement of AQP9 in hapten-induced contact hypersensitivity (CHS), as a murine model of skin allergic contact dermatitis, using AQP9 knockout (AQP9(-/-)) mice. First, the CHS response to hapten dinitrofluorobenzene (DNFB) was impaired in AQP9(-/-) mice compared with wild-type (WT) mice. Adoptive transfer of sensitized AQP9(-/-) draining lymph node (dLN) cells into WT recipients resulted in a reduced CHS response, indicating impaired sensitization in AQP9(-/-) mice. Second, administration of WT neutrophils into AQP9(-/-) mice during sensitization rescued the impaired CHS response. Neutrophil recruitment to dLNs upon hapten application was attenuated by AQP9 deficiency. Coincidentally, AQP9(-/-) neutrophils showed a reduced CC-chemokine receptor 7 (CCR7) ligand-induced migration efficacy, which was attributed to the attenuated recruitment of neutrophils to dLNs. Furthermore, we found that neutrophil deficiency, observed in AQP9(-/-) or neutrophil-depleted mice, decreased IL-17A production by dLN cells, which might be responsible for T cell activation during a subsequent CHS response. Taken together, these findings suggest that AQP9 is required for the development of sensitization during cutaneous acquired immune responses via regulating neutrophil function.

Indexed as

AnimalsAquaporinsCell MovementDermatitis, ContactDinitrofluorobenzeneImmunity, CellularLigandsLymph NodesLymphocyte ActivationMiceMice, KnockoutNeutrophilsReceptors, CCR7SkinAqp9 protein, mouseAquaporinsCcr7 protein, mouseDinitrofluorobenzeneLigandsReceptors, CCR7

Identifiers

PMID26489517
PMCPMC4614820
OpenAlexW2180606533

What OpenQuestion holds

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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.