Evidence map›Paper›PMID 24917456›Full record

ArticleMucosal immunology2015

A role for CCL28-CCR3 in T-cell homing to the human upper airway mucosa.

E Danilova, I Skrindo, E Gran, B J Hales, W A Smith, J Jahnsen, F E Johansen, F L Jahnsen, E S Baekkevold

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In one paragraph

Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 43 citations in OpenAlex.

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  16. Mechanisms of T cell organotropism.Cellular and molecular life sciences : CMLS · 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 4 institutions in 2 countries.

E DanilovaDepartment of Pathology and Centre for Immune Regulation (CIR), Oslo University Hospital-Rikshospitalet and University of Oslo, Oslo, Norway.
I Skrindo1] Department of Pathology and Centre for Immune Regulation (CIR), Oslo University Hospital-Rikshospitalet and University of Oslo, Oslo, Norway [2] Department of Otorhinolaryngology, Akershus University Hospital, Nordbyhagen, Norway.
E GranDepartment of Otolaryngology, Lovisenberg Diakonale Hospital, Oslo, Norway.
B J HalesCentre for Child Health Research, University of Western Australia, Telethon Institute for Child Health Research, Subiaco, Western Australia, Australia.
W A SmithCentre for Child Health Research, University of Western Australia, Telethon Institute for Child Health Research, Subiaco, Western Australia, Australia.
J JahnsenDepartment of Gastroenterology, Akershus University Hospital, Nordbyhagen, Norway.
F E Johansen1] Department of Pathology and Centre for Immune Regulation (CIR), Oslo University Hospital-Rikshospitalet and University of Oslo, Oslo, Norway [2] Department of Biosciences, University of Oslo, Oslo, Norway.
F L JahnsenDepartment of Pathology and Centre for Immune Regulation (CIR), Oslo University Hospital-Rikshospitalet and University of Oslo, Oslo, Norway.
E S BaekkevoldDepartment of Pathology and Centre for Immune Regulation (CIR), Oslo University Hospital-Rikshospitalet and University of Oslo, Oslo, Norway.
Oslo University Hospital · NOThe Kids Research Institute Australia · AUAkershus University Hospital · NOLovisenberg Diakonale Sykehus · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphocyte recruitment to peripheral tissues is fundamental for immune surveillance and homeostasis, but the chemokines and chemokine receptors responsible for tissue-specific homing of T cells to the upper airway mucosa have not been determined. To address this, we analyzed the chemokines expressed in the normal human nasal mucosa and found that CCL28 is preferentially expressed at a high level on the lumenal face of vascular endothelial cells in the mucosa. Analysis of the cognate chemokine receptors revealed that close to 50% of the CD4(+) T cells in the human nasal mucosa expressed the CCL28 receptor CCR3, whereas CCR3 was hardly detectable on T cells in the small intestine and skin. In the circulation, CCR3(+) T cells comprised a small subset that did not express homing receptors to the intestine or skin. Moreover, depletion of CCR3(+)CD4(+) T cells abrogated the proliferative response of human blood CD4(+) T cells against the opportunistic nasopharyngeal pathogen Haemophilus influenzae, indicating that the CCR3(+)CD4(+) T-cell subset in the circulation contains antigen specificities relevant for the upper airways. Together, these findings indicate that CCL28-CCR3 interactions are involved in the homeostatic trafficking of CD4(+) T cells to the upper airways.

Indexed as

AdultAgedAntigens, BacterialCD4-Positive T-LymphocytesCell MovementCell ProliferationCells, CulturedChemokines, CCEndothelium, VascularFemaleHaemophilus influenzaeHumansLymphocyte ActivationLymphocyte DepletionMaleMiddle AgedAntigens, BacterialCCL28 protein, humanCCR3 protein, humanChemokines, CCReceptors, CCR3Receptors, Lymphocyte Homing

Identifiers

PMID24917456
OpenAlexW1998769407

What OpenQuestion holds

Textmetadata
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.