Evidence map›Paper›PMID 31591201›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

IL-37 is increased in brains of children with autism spectrum disorder and inhibits human microglia stimulated by neurotensin.

Irene Tsilioni, Arti B Patel, Harry Pantazopoulos, Sabina Berretta, Pio Conti, Susan E Leeman, Theoharis C Theoharides

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.9field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

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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 4 institutions in 2 countries.

Irene TsilioniLaboratory of Molecular Immunopharmacology and Drug Discovery, Department of Immunology, Tufts University School of Medicine, Boston, MA 02111.
Arti B PatelLaboratory of Molecular Immunopharmacology and Drug Discovery, Department of Immunology, Tufts University School of Medicine, Boston, MA 02111.
Harry PantazopoulosTranslational Neuroscience Laboratory, McLean Hospital, Harvard Medical School, Belmont, MA 02478.
Sabina BerrettaTranslational Neuroscience Laboratory, McLean Hospital, Harvard Medical School, Belmont, MA 02478.
Pio ContiImmunology Division, Postgraduate Medical School, University of Chieti, 65100 Pescara, Italy.
Susan E LeemanDepartment of Pharmacology, Boston University School of Medicine, Boston, MA 02118; sleeman@bu.edu theoharis.theoharides@tufts.edu.ORCID 0000-0003-2875-1394
Theoharis C TheoharidesLaboratory of Molecular Immunopharmacology and Drug Discovery, Department of Immunology, Tufts University School of Medicine, Boston, MA 02111; sleeman@bu.edu theoharis.theoharides@tufts.edu.
Tufts University · USHarvard University · USBoston University · USUniversity of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) does not have a distinct pathogenesis or effective treatment. Increasing evidence supports the presence of immune dysfunction and inflammation in the brains of children with ASD. In this report, we present data that gene expression of the antiinflammatory cytokine IL-37, as well as of the proinflammatory cytokines IL-18 and TNF, is increased in the amygdala and dorsolateral prefrontal cortex of children with ASD as compared to non-ASD controls. Gene expression of IL-18R, which is a receptor for both IL-18 and IL-37, is also increased in the same brain areas of children with ASD. Interestingly, gene expression of the NTR3/sortilin receptor is reduced in the amygdala and dorsolateral prefrontal cortex. Pretreatment of cultured human microglia from normal adult brains with human recombinant IL-37 (1 to 100 ng/mL) inhibits neurotensin (NT)-stimulated secretion and gene expression of IL-1β and CXCL8. Another key finding is that NT, as well as the proinflammatory cytokines IL-1β and TNF increase IL-37 gene expression in cultured human microglia. The data presented here highlight the connection between inflammation and ASD, supporting the development of IL-37 as a potential therapeutic agent of ASD.

Indexed as

Adaptor Proteins, Vesicular TransportAmygdalaAutism Spectrum DisorderCells, CulturedChildHumansInterleukin-1Interleukin-18Interleukin-18 Receptor alpha SubunitInterleukin-1betaInterleukin-8MicrogliaNeurotensinPrefrontal CortexSortilinTumor Necrosis Factor-alphaAdaptor Proteins, Vesicular TransportCXCL8 protein, humanIL18R1 protein, humanIL1B protein, humanIL37 protein, humanInterleukin-1Interleukin-18Interleukin-18 Receptor alpha SubunitInterleukin-1betaInterleukin-8NeurotensinSortilinTNF protein, humanTumor Necrosis Factor-alphaautism spectrum disorderbrainIL-37inflammationneurotensin

Identifiers

PMID31591201
PMCPMC6815178
OpenAlexW2979471107

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.