Evidence map›Paper›PMID 38547647›Full record

ArticleRedox biology2024

NCF4 regulates antigen presentation of cysteine peptides by intracellular oxidative response and restricts activation of autoreactive and arthritogenic T cells.

Jing Xu, Chang He, Yongsong Cai, Xipeng Wang, Jidong Yan, Jing Zhang, Fujun Zhang, Vilma Urbonaviciute, Yuanyuan Cheng, Shemin Lu and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. 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

11 authors at 4 institutions in 3 countries.

Jing XuNational Joint Engineering Research Center of Biodiagnostics and Biotherapy, and Department of Rheumatology, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, PR China; Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China; Medical Inflammation Research, Division of Immunology, Dept. of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Chang HeKey Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China; Medical Inflammation Research, Division of Immunology, Dept. of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden; Department of Cardiology, The Second Affiliated Hospital, Zhejiang University Schoole of Medicine, Zhejiang, Hangzhou, PR China.
Yongsong CaiDepartment of Joint Surgery, Xi'an Honghui Hospital, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China.
Xipeng WangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China.
Jidong YanDepartment of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 710061, Xi'an, PR China.
Jing ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China.
Fujun ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China.
Vilma UrbonaviciuteMedical Inflammation Research, Division of Immunology, Dept. of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden.
Yuanyuan ChengNational Joint Engineering Research Center of Biodiagnostics and Biotherapy, and Department of Rheumatology, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, PR China.
Shemin LuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China.
Rikard HolmdahlNational Joint Engineering Research Center of Biodiagnostics and Biotherapy, and Department of Rheumatology, Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, 710004, PR China; Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education, Xi'an, Shaanxi, 710061, PR China; Medical Inflammation Research, Division of Immunology, Dept. of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden. Electronic address: rikard.holmdahl@ki.se.
Xi'an Jiaotong University · CNKarolinska Institutet · SESecond Affiliated Hospital of Xi'an Jiaotong University · CNXi'an Honghui Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases, such as rheumatoid arthritis (RA) and systemic lupus erythematous, are regulated by polymorphisms in genes contributing to the NOX2 complex. Mutations in both Ncf1 and Ncf4 affect development of arthritis in experimental models of RA, but the different regulatory pathways mediated by NOX2-derived reactive oxygen species (ROS) have not yet been clarified. Here we address the possibility that intracellular ROS, regulated by the NCF4 protein (earlier often denoted p40phox) which interacts with endosomal membranes, could play an important role in the oxidation of cysteine peptides in mononuclear phagocytic cells, thereby regulating antigen presentation and activation of arthritogenic T cells. To study the role of NCF4 we used mice with an amino acid replacing mutation (NCF4

Indexed as

Antigen PresentationCysteineLymphocyte ActivationOxidation-ReductionReactive Oxygen SpeciesT-LymphocytesAnimalsArthritis, RheumatoidMacrophagesMiceNADPH OxidasesPeptidesCysteineNADPH OxidasesPeptidesReactive Oxygen SpeciesAntigen presentationArthritisIntracellular reactive oxygen speciesNeutrophil cytosolic factor 1 (NCF1, earlier often denoted p47phox)Neutrophil cytosolic factor 4 (NCF4, earlier often denoted p40phox)Redox regulationT cell activation

Identifiers

PMID38547647
PMCPMC11096609
OpenAlexW4393204193

What OpenQuestion holds

Textmetadata
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.