Evidence map›Paper›PMID 37894952›Full record

ArticleInternational journal of molecular sciences2023

Histamine H4 Receptor Antagonist Ameliorates the Progression of Experimental Autoimmune Encephalomyelitis via Regulation of T-Cell Imbalance.

Abdullah A Aldossari, Mohammed A Assiri, Mushtaq A Ansari, Ahmed Nadeem, Sabry M Attia, Saleh A Bakheet, Thamer H Albekairi, Hatun A Alomar, Haneen A Al-Mazroua, Taghreed N Almanaa and 3 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.0field-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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
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

13 authors at 1 institution in 1 country.

Abdullah A AldossariDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0001-8776-1088
Mohammed A AssiriDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-9527-229X
Mushtaq A AnsariDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-3556-5939
Ahmed NadeemDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0003-2038-8367
Sabry M AttiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0001-8560-8944
Saleh A BakheetDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Thamer H AlbekairiDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Hatun A AlomarDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0001-7495-0592
Haneen A Al-MazrouaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-5838-3468
Taghreed N AlmanaaDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.
Mohammed A Al-HamamahDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Mohammad Y AlwetaidDepartment of Botany and Microbiology, College of Science, King Saud University, Riyadh 11451, Saudi Arabia.
Sheikh F AhmadDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.ORCID 0000-0002-8282-3726
King Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a degenerative condition characterized by immune-mediated attacks on the central nervous system (CNS), resulting in demyelination and recurring T-cell responses. The histamine H4 receptor (H4R) is mainly expressed in cellular populations and plays a vital role in inflammation and immunological responses. The role of H4R in neurons of the CNS has recently been revealed. However, the precise role of H4R in neuronal function remains inadequately understood. The objective of this work was to investigate the impact of JNJ 10191584 (JNJ), a highly effective and specific H4R antagonist, on the development of experimental autoimmune encephalomyelitis (EAE) and to gain insight into the underlying mechanism involved. In this study, we examined the potential impact of JNJ therapy on the course of EAE in SJL/J mice. EAE mice were administered an oral dose of JNJ at a concentration of 6 mg/kg once a day, starting from day 10 and continuing until day 42. Afterward, the mice's clinical scores were assessed. In this study, we conducted additional research to examine the impact of JNJ on several types of immune cells, specifically Th1 (IFN-γ and T-bet), Th9 (IL-9 and IRF4), Th17 (IL-17A and RORγt), and regulatory T (Tregs; Foxp3 and TGF-β1) cells in the spleen. In this study, we further investigated the impact of JNJ on the mRNA expression levels of

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsForkhead Transcription FactorsHistamine AntagonistsInterleukin-17Interleukin-9MiceMice, Inbred C57BLNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Histamine H4Transforming Growth Factor beta1Forkhead Transcription FactorsHistamine AntagonistsInterleukin-17Interleukin-9Nuclear Receptor Subfamily 1, Group F, Member 3Receptors, Histamine H4Transforming Growth Factor beta1EAEH4R antagonistinflammatory mediators transcription factorsJNJ 10191584multiple sclerosis

Identifiers

PMID37894952
PMCPMC10607370
OpenAlexW4387706608

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.