Evidence map›Paper›PMID 30127782›Full record

ArticleFrontiers in immunology2018

Peripheral T Cell Depletion by FTY720 Exacerbates Hypoxic-Ischemic Brain Injury in Neonatal Mice.

Josephine Herz, Christian Köster, Marius Crasmöller, Hanna Abberger, Wiebke Hansen, Ursula Felderhoff-Müser, Ivo Bendix

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

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  10. The Effects of Fingolimod (FTY720) on Leukocyte Subset Circulation cannot be Behaviourally Conditioned in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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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

7 authors at 1 institution in 1 country.

Josephine HerzDepartment of Pediatrics 1, Neonatology and Experimental Perinatal Neuroscience, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Christian KösterDepartment of Pediatrics 1, Neonatology and Experimental Perinatal Neuroscience, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Marius CrasmöllerDepartment of Pediatrics 1, Neonatology and Experimental Perinatal Neuroscience, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Hanna AbbergerInstitute of Medical Microbiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Wiebke HansenInstitute of Medical Microbiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Ursula Felderhoff-MüserDepartment of Pediatrics 1, Neonatology and Experimental Perinatal Neuroscience, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
Ivo BendixDepartment of Pediatrics 1, Neonatology and Experimental Perinatal Neuroscience, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxic-ischemic injury to the developing brain remains a major cause of significant long-term morbidity and mortality. Emerging evidence from neonatal brain injury models suggests a detrimental role for peripheral lymphocytes. The immunomodulatory substance FTY720, a sphingosine-1-phosphate receptor agonist, was shown to reduce adult ischemia-induced neurodegeneration through its lymphopenic mode of action. In the present study, we hypothesized that FTY720 promotes neuroprotection by reducing peripheral lymphocytes and their infiltration into the injured neonatal brain. Term-born equivalent postnatal day 9 C57BL/6 mice were exposed to hypoxia ischemia (HI) followed by a single injection of 1 mg/kg FTY720 or vehicle (0.9% sodium chloride). Brain injury, microglia, and endothelial activation were assessed 7 days post HI using histology and western blot. Peripheral and cerebral leukocyte subsets were analyzed by multichannel flow cytometry. Whether FTY720s' effects could be attributed to its lymphopenic mode of action was determined in T cell-depleted mice. In contrast to our hypothesis, FTY720 exacerbated HI-induced neuropathology including loss of gray and white matter structures. While microglia and endothelial activation remained unchanged, FTY720 induced a strong and sustained depletion of peripheral T cells resulting in significantly reduced cerebral infiltration of CD4 T cells. CD4 T cell subset analysis revealed that circulating regulatory and effector T cells counts were similarly decreased after FTY720 treatment. However, since neonatal HI

Indexed as

Lymphocyte DepletionAnimalsAnimals, NewbornBrainFemaleFingolimod HydrochlorideHypoxia-Ischemia, BrainImmunosuppressive AgentsInflammationLymphocyte SubsetsMaleMiceMice, Inbred C57BLNeuroprotective AgentsReceptors, LysosphingolipidT-LymphocytesFingolimod HydrochlorideImmunosuppressive AgentsNeuroprotective AgentsReceptors, Lysosphingolipidbirth asphyxiabrain injuryFTY720immune cell infiltrationneonatal hypoxia ischemianeuroinflammationT cells

Identifiers

PMID30127782
PMCPMC6087766
OpenAlexW2887563890

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.