Evidence map›Paper›PMID 29243317›Full record

ReviewAmerican journal of reproductive immunology (New York, N.Y. : 1989)2018

IL-17 in neonatal health and disease.

Shelley M Lawrence, Jessica Lauren Ruoss, James L Wynn

Open access · greenAbstract readReview
In one paragraph

Review in American journal of reproductive immunology (New York, N.Y. : 1989), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Perturbation of the Preterm Human Immune System in Early Life.medRxiv : the preprint server for health sciences · 2025
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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

3 authors at 2 institutions in 1 country.

Shelley M LawrenceDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, College of Medicine, University of California, San Diego, La Jolla, CA, USA.ORCID 0000-0001-5608-7051
Jessica Lauren RuossDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL, USA.
James L WynnDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, College of Medicine, University of Florida, Gainesville, FL, USA.
University of Florida · USUniversity of California San Diego · US

Funding

Microfluidic Assessment of Clinical Outcomes in Preterm NewbornsR01HD089939 · NICHD · UNIVERSITY OF FLORIDA · PI IRIMIA, DANIEL, MOLDAWER, LYLE L · 2017 to 2021
$3.3M
Modifiable Determinants of Mortality in Neonatal SepsisR01GM128452 · NIGMS · UNIVERSITY OF FLORIDA · PI WYNN, JAMES LAWRENCE · 2018 to 2022
$1.9M
The Role of the Inflammasome in Neonatal SepsisK08GM106143 · NIGMS · VANDERBILT UNIVERSITY · PI WYNN, JAMES LAWRENCE · 2013 to 2017
$875k
NICHD NIH HHS R01 HD089939NIGMS NIH HHS K08 GM106143NIGMS NIH HHS R01 GM128452
6 · The paper itself

Abstract

Over the last few years, scientific interest in the cytokine IL-17A has intensified as its role in human health and disease has been elucidated. Discovered almost a quarter century ago, IL-17A is known to have poor biologic activity when acting alone, but attains robust actions when working synergistically with potent mediators of proinflammatory immune responses, such as IL-6 and IL-8. IL-17A is produced by specialized innate immune cells that protect host barriers from the outside world. Like sentries, these innate immune cells can "sound the alarm" through increased production of IL-17A, causing activation and recruitment of primed neutrophils and monocytes when pathogens escape initial host defenses. In this way, IL-17A promulgates mechanisms responsible for pathogen death and clearance. However, when IL-17A pathways are triggered during fetal development, due to chorioamnionitis or in utero inflammatory conditions, IL-17A can instigate and/or exacerbate fetal inflammatory responses that increase neonatal morbidities and mortality associated with common neonatal conditions such as sepsis, bronchopulmonary dysplasia (BPD), patent ductus arteriosus (PDA), and necrotizing enterocolitis (NEC). This review details the ontogeny of IL-17A in the fetus and newborn, discusses how derangements in its production can lead to pathology, and describes known and evolving therapies that may attenuate IL-17A-mediated human conditions.

Indexed as

AnimalsHumansImmunity, InnateInfant HealthInfant, NewbornInfant, Newborn, DiseasesInflammationInterleukin-17Interleukin-17bronchopulmonary dysplasiaIL-17necrotizing enterocolitispatent ductus arteriosusretinopathy of prematuritysepsis

Identifiers

PMID29243317
PMCPMC6051706
OpenAlexW2772040342

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.