Evidence map›Paper›PMID 40274824›Full record

ArticleNature communications2025

Neutrophil single-cell analysis identifies a type II interferon-related subset for predicting relapse of autoimmune small vessel vasculitis.

Masayuki Nishide, Kei Nishimura, Hiroaki Matsushita, Shoji Kawada, Hiroshi Shimagami, Shoichi Metsugi, Yasuhiro Kato, Takahiro Kawasaki, Kohei Tsujimoto, Ryuya Edahiro and 10 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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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

20 authors.

Masayuki Nishide *Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan. nishide@imed3.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-6060-1228
Kei Nishimura *Department of Advanced Clinical and Translational Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Hiroaki MatsushitaDepartment of Advanced Clinical and Translational Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Shoji KawadaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Hiroshi ShimagamiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Shoichi MetsugiDepartment of Advanced Clinical and Translational Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Yasuhiro KatoDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0002-4050-2350
Takahiro KawasakiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Kohei TsujimotoDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Ryuya EdahiroDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Yuya ShiraiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0002-0518-9020
Eri ItotagawaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Maiko NaitoDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0002-4360-7043
Yuji YamamotoDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0002-5489-5079
Kazuki MatsukawaDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Ryusuke OmiyaJoint Research Chair of Innovative Drug Discovery in Immunology, World Premier International Research Center Initiative (WPI), Immunology Frontier Research Center (IFReC), Osaka University, Suita, Osaka, Japan.
Yukinori OkadaDepartment of Statistical Genetics, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.ORCID http://orcid.org/0000-0002-0311-8472
Kunihiro HattoriJoint Research Chair of Innovative Drug Discovery in Immunology, World Premier International Research Center Initiative (WPI), Immunology Frontier Research Center (IFReC), Osaka University, Suita, Osaka, Japan.
Masashi NarazakiDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Atsushi KumanogohDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan. kumanogo@imed3.med.osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-4749-7117

Funding

MEXT | Japan Science and Technology Agency (JST) JPMJFR235BMEXT | Japan Society for the Promotion of Science (JSPS) JP24K11596
6 · The paper itself

Abstract

To identify the dynamics of neutrophil autoimmunity, here we focus on anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis and perform single-cell transcriptome and surface proteome analyses on peripheral white blood cells from patients with new-onset microscopic polyangiitis (MPA). Compared with controls, two neutrophil populations, immature neutrophils and neutrophils with type II interferon signature genes (Neu_T2ISG), are increased in patients with MPA. Trajectory and cell-cell interaction analyses identify Neu_T2ISG as a subset that differentiates from mature neutrophils upon stimulation with IFN-γ and TNF, which synergize to induce myeloperoxidase and Fcγ receptors expression on the neutrophil cell surface and promote ANCA-induced neutrophil extracellular trap formation. Case-by-case analysis indicates that patients with a high proportion of the Neu_T2ISG subset are associated with persistent vasculitis symptoms. A larger cohort analysis shows that serum IFN-γ levels at disease onset correlate with susceptibility to disease relapse. Our findings thus identify neutrophil diversity at the single cell level and implicate a biomarker for predicting relapse in small vessel vasculitis.

Indexed as

Anti-Neutrophil Cytoplasmic Antibody-Associated VasculitisInterferon-gammaMicroscopic PolyangiitisNeutrophilsAdultAgedAntibodies, Antineutrophil CytoplasmicBiomarkersCase-Control StudiesExtracellular TrapsFemaleHumansMaleMiddle AgedPeroxidaseReceptors, IgGAntibodies, Antineutrophil CytoplasmicBiomarkersInterferon-gammaPeroxidaseReceptors, IgGTumor Necrosis Factor-alpha

Identifiers

PMID40274824
PMCPMC12022166

What OpenQuestion holds

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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.