Evidence map›Paper›PMID 33927721›Full record

ArticleFrontiers in immunology2021

Baricitinib Ameliorates Experimental Autoimmune Encephalomyelitis by Modulating the Janus Kinase/Signal Transducer and Activator of Transcription Signaling Pathway.

Chun Dang, Yaoheng Lu, Xingyu Chen, Qian Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  14. Direct Effects of the Janus Kinase Inhibitor Baricitinib on Sensory Neurons.International journal of molecular sciences · 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

4 authors at 3 institutions in 1 country.

Chun DangWest China Medical Publishers, West China Hospital, Sichuan University, Chengdu, China.
Yaoheng LuDepartment of General Surgery, Chengdu Integrated Traditional Chinese Medicine & Western Medicine Hospital, Chengdu, China.
Xingyu ChenDepartment of General Surgery, Chengdu Integrated Traditional Chinese Medicine & Western Medicine Hospital, Chengdu, China.
Qian LiDepartment of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Chengdu University of Traditional Chinese Medicine · CNSecond Affiliated Hospital of Harbin Medical University · CNWest China Medical Center of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS) and a CD4+ T cell-mediated autoimmune disease. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is recognized as the major mechanism that regulates the differentiation and function of T helper (Th) 1 and Th17 cells, which are recognized as pivotal effector cells responsible for the development of EAE. We used baricitinib, a JAK 1/2 inhibitor, to investigate the therapeutic efficacy of inhibiting the JAK/STAT pathway in EAE mice. Our results showed that baricitinib significantly delayed the onset time, decreased the severity of clinical symptoms, shortened the duration of EAE, and alleviated demyelination and immune cell infiltration in the spinal cord. In addition, baricitinib treatment downregulated the proportion of interferon-γ+CD4+ Th1 and interleukin-17+CD4+ Th17 cells, decreased the levels of retinoic acid-related orphan receptor γ t and T-bet mRNA, inhibited lymphocyte proliferation, and decreased the expression of proinflammatory cytokines and chemokines in the spleen of mice with EAE. Furthermore, our results showed the role of baricitinib in suppressing the phosphorylation of STATs 1, 3, and 4 in the spleen of EAE mice. Therefore, our study demonstrates that baricitinib could potentially alleviate inflammation in mice with EAE and may be a promising candidate for treating MS.

Indexed as

Administration, OralAnimalsAzetidinesCD4-Positive T-LymphocytesCell ProliferationCells, CulturedCytokinesEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFemaleGene ExpressionJanus KinasesMiceMice, Inbred C57BLPurinesPyrazolesAzetidinesbaricitinibCytokinesJanus KinasesPurinesPyrazolesSTAT Transcription FactorsSulfonamidesbaricitinibEAEJAK/STATTh1Th17Th1/Th17

Identifiers

PMID33927721
PMCPMC8076548
OpenAlexW3154233248

What OpenQuestion holds

Textmetadata
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.