Evidence map›Paper›PMID 29382365›Full record

ArticleArthritis research & therapy2018

Increase of MZB1 in B cells in systemic lupus erythematosus: proteomic analysis of biopsied lymph nodes.

Aya Miyagawa-Hayashino, Hajime Yoshifuji, Koji Kitagori, Shinji Ito, Takuma Oku, Yoshitaka Hirayama, Adeeb Salah, Toshiki Nakajima, Kaori Kiso, Norishige Yamada and 2 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.0field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 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

12 authors at 3 institutions in 1 country.

Aya Miyagawa-HayashinoCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan. ayam@kuhp.kyoto-u.ac.jp.
Hajime YoshifujiDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Koji KitagoriCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan.
Shinji ItoBio Frontier Platform, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takuma OkuCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan.
Yoshitaka HirayamaCenter for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan.
Adeeb SalahDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Toshiki NakajimaDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kaori KisoCenter for Anatomical, Pathological and Forensic Medical Research, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Norishige YamadaCenter for Anatomical, Pathological and Forensic Medical Research, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hironori HagaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Tatsuaki TsuruyamaCenter for Anatomical, Pathological and Forensic Medical Research, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kyoto University · JPKyoto University Hospital · JPKyoto City Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus (SLE) is a prototypical autoimmune disease in which dysregulation of B cells has been recognized. Here, we searched for potential biomarkers of SLE using liquid chromatography-tandem mass spectrometry (LC-MS).

methodsLymph nodes from SLE patients and controls were analyzed by LC-MS. To validate the identified molecules, immunoblotting and immunohistochemistry were performed and B cells from SLE patients were analyzed by quantitative RT-PCR. B-cell subsets from NZB/W F1 mice, which exhibit autoimmune disease resembling human SLE, were analyzed by flow cytometry. Endoplasmic reticulum (ER) stress was induced by tunicamycin and the serum concentration of anti-dsDNA antibodies was determined by ELISA. TUNEL methods and immunoblotting were used to assess the effect of tunicamycin.

resultsMZB1, which comprises part of a B-cell-specific ER chaperone complex and is a key player in antibody secretion, was one of the differentially expressed proteins identified by LC-MS and confirmed by immunoblotting. Immunohistochemically, larger numbers of MZB1

conclusionsMZB1 may be a potential therapeutic target in excessive antibody-secreting cells in SLE.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisB-LymphocytesChromatography, LiquidCytokinesHumansLupus Erythematosus, SystemicLymph NodesMass SpectrometryMice, Inbred C57BLMice, Inbred NZBProteomeProteomicsTunicamycinAdaptor Proteins, Signal TransducingCytokinesMZB1 protein, humanProteomeTunicamycinFormalin-fixed paraffin-embeddedLupus-prone miceProteomic analysisSLE lymphadenopathySystemic lupus erythematosusTUNELUnfolded protein response

Identifiers

PMID29382365
PMCPMC5791339
OpenAlexW2794288507

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.