Evidence map›Paper›PMID 32764561›Full record

ArticleScientific reports2020

Mitochondrial DNA enhance innate immune responses in neuromyelitis optica by monocyte recruitment and activation.

Mikito Shimizu, Tatsusada Okuno, Makoto Kinoshita, Hisae Sumi, Harutoshi Fujimura, Kazuya Yamashita, Tomoyuki Sugimoto, Shuhei Sakakibara, Kaori Sakakibara, Toru Koda and 9 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 16 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

19 authors at 4 institutions in 1 country.

Mikito Shimizu *Department of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Tatsusada Okuno *Department of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan. okuno@neurol.med.osaka-u.ac.jp.
Makoto Kinoshita *Department of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hisae SumiDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Harutoshi FujimuraDepartment of Neurology, Osaka-Toneyama National Medical Center, 5-1-1, Toneyama, Toyonaka, Osaka, 560-8552, Japan.
Kazuya YamashitaDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Tomoyuki SugimotoFaculty of Data Science, Shiga University, 1-1-1, Baba, Hikone, Shiga, 522-8522, Japan.
Shuhei SakakibaraLaboratory of Immune Regulation, Immunology Frontier Research Center, Osaka University, 3-1, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Kaori SakakibaraDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Toru KodaDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Satoru TadaDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Teruyuki IshikuraDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hisashi MurataDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shohei BeppuDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Naoyuki ShiraishiDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yasuko SugiyamaDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yuji NakatsujiDepartment of Neurology, Faculty of Medicine, University of Toyama, 2630, Sugitani, Toyama, 930-0194, Japan.
Atsushi KumanogohDepartment of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hideki MochizukiDepartment of Neurology, Osaka University Graduate School of Medicine, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
Osaka University · JPShiga University · JPToneyama National Hospital · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although recent studies indicate the involvement of monocytes in accelerating the lesion formation of neuromyelitis optica spectrum disorder (NMOSD), the precise mechanism of the innate immune system activation remains elusive. Thus, in this study, we aimed to clarify the mechanisms of NMOSD pathogenesis from the viewpoint of innate immunity activation. We established anti-AQP4 recombinant autoantibodies (Ab) from plasmablasts in NMOSD patient's CSF. Human astrocytes treated with anti-AQP4 Ab produced a significant amount of CCL2 and contributed to the efficient recruitment of monocytes. Moreover, mitochondrial DNA (mtDNA), which activated monocytes via Toll-like receptor 9 (TLR9), was released from astrocytes treated with anti-AQP4 Ab. MtDNA further enhanced CCL2 production by monocytes, and it was demonstrated that mtDNA concentration correlated with the efficiency of monocyte recruitment in the CSF of NMOSD patients. In conclusion, these observations highlight that mtDNA which was released from astrocytes damaged by anti-AQP4 Ab has a central role in establishing the inflammatory loop of monocyte recruitment and activation via an innate immunity pathway.

Indexed as

AdultAgedAntibodiesAquaporin 4AstrocytesChemokine CCL2DNA, MitochondrialFemaleHEK293 CellsHumansImmunity, InnateMiddle AgedMitochondriaMonocytesNeuromyelitis OpticaToll-Like Receptor 9AntibodiesAQP4 protein, humanAquaporin 4CCL2 protein, humanChemokine CCL2DNA, MitochondrialTLR9 protein, humanToll-Like Receptor 9

Identifiers

PMID32764561
PMCPMC7414017
OpenAlexW3047583143

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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.