Evidence map›Paper›PMID 39563375›Full record

ArticleJournal of neuroinflammation2024

IL-37 suppresses CNS autoimmunity by increasing the frequency of Treg cells and reducing CD4 + T cell-derived IL-10 production.

Reza Yazdani, Hamed Naziri, Gholamreza Azizi, Bogoljub Ciric, Mozhde Askari, Amir Moghadam Ahmadi, Jaya Aseervatham, Guang-Xian Zhang, Abdolmohamad Rostami

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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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.

Reza YazdaniDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Hamed NaziriDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Gholamreza AziziDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Bogoljub CiricDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Mozhde AskariDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Amir Moghadam AhmadiDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Jaya AseervathamDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Guang-Xian ZhangDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA.
Abdolmohamad RostamiDepartment of Neurology, Thomas Jefferson University, 900 Walnut Street, Suite 300, Philadelphia, PA, 19107, USA. a.m.rostami@jefferson.edu.

Funding

IL-37: a novel regulator of inflammation in CNS autoimmunityR01AI160189 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI A.M. Rostami · 2021 to 2026
$1.9M
Role of IL-7R in CNS autoimmunityR01AI156384 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI A.M. Rostami · 2021 to 2026
$1.9M
NIAID NIH HHS R01 AI156384NIAID NIH HHS R01 AI160189
6 · The paper itself

Abstract

backgroundInterleukin-37 (IL-37) has anti-inflammatory properties in innate and adaptive immunity. Patients with multiple sclerosis (MS), an autoimmune inflammatory demyelinating disease of the central nervous system (CNS), have increased serum levels of IL-37. However, it is unknown whether IL-37 has an inhibitory effect on ongoing autoimmune neuroinflammation, thus offering a potential MS therapy.

aimHere, we examined the effect of IL-37 in an experimental autoimmune encephalomyelitis (EAE) model after disease onset to determine if it was protective.

findingsIL-37-treated mice developed a less severe disease than control mice, with reduced demyelination as determined by increased expression of myelin basic protein. IL-37 suppressed inflammation by decreasing infiltration of CD4 + T cells into the CNS and increasing the frequency of regulatory T cells, while IL-10 expression by CD4 + T cells decreased over time in the CNS.

conclusionOur findings confirm the immunomodulatory role of IL-37 in CNS inflammation during ongoing disease, thus indicating the potential of IL-37 as an inhibitory reagent for MS therapy.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalInterleukin-1Interleukin-10Mice, Inbred C57BLT-Lymphocytes, RegulatoryAnimalsAutoimmunityCD4-Positive T-LymphocytesCentral Nervous SystemFemaleMiceIL37 protein, humanInterleukin-1Interleukin-10Experimental autoimmune encephalomyelitis (EAE)IL-10IL-37InflammationMultiple sclerosis

Identifiers

PMID39563375
PMCPMC11575187

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Registered trials

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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.