Evidence map›Paper›PMID 38216632›Full record

ArticleScientific reports2024

Early involvement of peripherally derived monocytes in inflammation in an NMO-like mouse model.

Moonhang Kim, Won Seok Kim, Hyeuk Cha, Boram Kim, Young Nam Kwon, Sung Min Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

6 authors at 2 institutions in 1 country.

Moonhang KimBiomedical Research Institute, Seoul National University Hospital, Seoul, 03082, Republic of Korea. mook1052@gmail.com.
Won Seok KimBiomedical Research Institute, Seoul National University Hospital, Seoul, 03082, Republic of Korea.
Hyeuk ChaBiomedical Research Institute, Seoul National University Hospital, Seoul, 03082, Republic of Korea.
Boram KimBiomedical Research Institute, Seoul National University Hospital, Seoul, 03082, Republic of Korea.
Young Nam KwonDepartment of Neurology, Severance Hospital, Yonsei University College of Medicine, Seoul, 03722, Republic of Korea.
Sung Min KimDepartment of Neurology, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea. sueh916@gmail.com.
Seoul National University Hospital · KRYonsei University · KR

Funding

Ministry of Science and ICT, South Korea NRF-2021R1C1C2012932
6 · The paper itself

Abstract

Neuromyelitis optica (NMO) is an autoimmune inflammatory disease that primarily affects the optic nerve and spinal cord within the central nervous system (CNS). Acute astrocyte injury caused by autoantibodies against aquaporin 4 (NMO-IgG) is a well-established key factor in the pathogenesis, ultimately leading to neuronal damage and patient disability. In addition to these humoral immune processes, numerous innate immune cells were found in the acute lesions of NMO patients. However, the origin and function of these innate immune cells remain unclear in NMO pathogenesis. Therefore, this study aims to analyze the origin and functions of these innate immune cells in an NMO-like mouse model and evaluate their role in the pathophysiology of NMO. The expression of Tmem119 on Iba1 + cells in brain tissue disappeared immediately after the injection of NMO-IgG + human complement mixture, while the expression of P2ry12 remained well-maintained at 1 day after injection. Based on these observations, it was demonstrated that monocytes infiltrate the brain during the early stages of the pathological process and are closely associated with the inflammatory response through the expression of the proinflammatory cytokine IL-1β. Understanding the variations in the expression patterns of P2ry12, Tmem119, and other markers could be helpful in distinguishing between these cell types and further analyzing their functions. Therefore, this research may contribute to a better understanding of the mechanisms and potential treatments for NMO.

Indexed as

Autoimmune DiseasesNeuromyelitis OpticaAnimalsAquaporin 4AutoantibodiesDisease Models, AnimalHumansImmunoglobulin GInflammationMiceMonocytesAquaporin 4AutoantibodiesImmunoglobulin G

Identifiers

PMID38216632
PMCPMC10786844
OpenAlexW4390827527

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.