Evidence map›Paper›PMID 27534549›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

IL-17 Promotes Neutrophil-Mediated Immunity by Activating Microvascular Pericytes and Not Endothelium.

Rebecca Liu, Holly M Lauridsen, Robert A Amezquita, Richard W Pierce, Dan Jane-Wit, Caodi Fang, Amanda S Pellowe, Nancy C Kirkiles-Smith, Anjelica L Gonzalez, Jordan S Pober

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
3.3field-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

74 citing papers in PubMed, 121 citations in OpenAlex.

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14 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Rebecca LiuDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;ORCID 0000-0002-3761-7018
Holly M LauridsenDepartment of Biomedical Engineering, Yale University, New Haven, CT 06520;ORCID 0000-0002-0880-1086
Robert A AmezquitaDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; Howard Hughes Medical Institute, Chevy Chase, MD 20815;ORCID 0000-0001-6868-7193
Richard W PierceDepartment of Pediatrics, Yale University School of Medicine, New Haven, CT 06520; and.
Dan Jane-WitDivision of Cardiology, Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516.
Caodi FangDivision of Cardiology, Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516.
Amanda S PelloweDepartment of Biomedical Engineering, Yale University, New Haven, CT 06520;
Nancy C Kirkiles-SmithDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;
Anjelica L GonzalezDepartment of Biomedical Engineering, Yale University, New Haven, CT 06520;
Jordan S PoberDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; jordan.pober@yale.edu.ORCID 0000-0001-5990-1071
Yale University · USVA Connecticut Healthcare System · USHoward Hughes Medical Institute · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Presentation of Alloantigen by Human Vascular CellsR01HL051014 · NHLBI · YALE UNIVERSITY · PI MANES, THOMAS DAVID, POBER, JORDAN S · 1994 to 2019
$10.4M
IMMUNOHEMATOLOGY/TRANSFUSION MEDICINE RESEARCH TRAININGT32HL007974 · NHLBI · YALE UNIVERSITY · PI JEANNE E HENDRICKSON, Diane S Krause · 2001 to 2026
$8.1M
Mechanisms of Non-Canonical NF-kB Activation in Transplant ArteriosclerosisR00HL125895 · NHLBI · YALE UNIVERSITY · PI JANE-WIT, DANIEL · 2017 to 2019
$732k
Modulation of Inflammation and Injury by IL-17-Activated PericytesF31HL129563 · NHLBI · YALE UNIVERSITY · PI LIU, REBECCA · 2015 to 2016
$56k
NCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA016359NHLBI NIH HHS F31 HL129563NHLBI NIH HHS R00 HL125895NHLBI NIH HHS R01 HL051014NHLBI NIH HHS T32 HL007974NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

A classical hallmark of acute inflammation is neutrophil infiltration of tissues, a multistep process that involves sequential cell-cell interactions of circulating leukocytes with IL-1- or TNF-activated microvascular endothelial cells (ECs) and pericytes (PCs) that form the wall of the postcapillary venules. The initial infiltrating cells accumulate perivascularly in close proximity to PCs. IL-17, a proinflammatory cytokine that acts on target cells via a heterodimeric receptor formed by IL-17RA and IL-17RC subunits, also promotes neutrophilic inflammation but its effects on vascular cells are less clear. We report that both cultured human ECs and PCs strongly express IL-17RC and, although neither cell type expresses much IL-17RA, PCs express significantly more than ECs. IL-17, alone or synergistically with TNF, significantly alters inflammatory gene expression in cultured human PCs but not ECs. RNA sequencing analysis identifies many IL-17-induced transcripts in PCs encoding proteins known to stimulate neutrophil-mediated immunity. Conditioned media from IL-17-activated PCs, but not ECs, induce pertussis toxin-sensitive neutrophil polarization, likely mediated by PC-secreted chemokines, and they also stimulate neutrophil production of proinflammatory molecules, including TNF, IL-1α, IL-1β, and IL-8. Furthermore, IL-17-activated PCs, but not ECs, can prolong neutrophil survival by producing G-CSF and GM-CSF, delaying the mitochondrial outer membrane permeabilization and caspase-9 activation. Importantly, neutrophils exhibit enhanced phagocytic capacity after activation by conditioned media from IL-17-treated PCs. We conclude that PCs, not ECs, are the major target of IL-17 within the microvessel wall and that IL-17-activated PCs can modulate neutrophil functions within the perivascular tissue space.

Indexed as

Caspase 9Cells, CulturedCulture MediaCytokinesEndothelium, VascularGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-17Neutrophil InfiltrationNeutrophilsPericytesReceptors, Interleukin-17Sequence Analysis, RNATumor Necrosis Factor-alphaVenulesCaspase 9Culture MediaCytokinesGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-17Receptors, Interleukin-17Tumor Necrosis Factor-alpha

Identifiers

PMID27534549
PMCPMC5010945
OpenAlexW2518502109

What OpenQuestion holds

Textmetadata
LicenceTDM
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.