Evidence map›Paper›PMID 39482663›Full record

ArticleBMC medicine2024

TM9SF1 expression correlates with autoimmune disease activity and regulates antibody production through mTOR-dependent autophagy.

Juan Xiao, Zhenwang Zhao, Fengqiao Zhou, Jinsong Xiong, Zean Yang, Baoxian Gong, Lei Xiang, Mingming Liu, Fengsheng Cao, Hong Xiao and 3 more

Abstract read
In one paragraph

Article in BMC medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
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  6. Review
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

13 authors.

Juan XiaoInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Zhenwang ZhaoInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Fengqiao ZhouInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Jinsong XiongGucheng People's Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441700, China.
Zean YangGucheng People's Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441700, China.
Baoxian GongGucheng People's Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441700, China.
Lei XiangInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Mingming LiuInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Fengsheng CaoInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Hong XiaoInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China.
Huabo ChenInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China. chenhb@hbuas.edu.cn.
Anbing ZhangInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China. xf_zab@sina.com.
Ke WangInstitute of Neuroscience and Brain Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, 441021, China. wangk201912@hbuas.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransmembrane 9 superfamily member 1 (TM9SF1) is involved in inflammation. Since both inflammatory and autoimmune diseases are linked to immune cells regulation, this study investigated the association between TM9SF1 expression and autoimmune disease activity. As B cell differentiation and autoantibody production exacerbate autoimmune disease, the signaling pathways involved in these processes were explored.

methodsTm9sf1

resultsThe Tm9sf1

conclusionsThe primary finding was the identification of the molecular mechanism underlying autophagy regulation in B cells, in which Tm9sf1 knockout was found to modulate mTOR-dependent autophagy to block B cell differentiation into antibody-secreting plasma cells. It was also found that TM9SF1 expression level in PBMCs was an accurate indicator of disease activity in patients with RA and SLE, suggesting its clinical potential for monitoring disease activity in these patients.

Indexed as

Arthritis, RheumatoidAutophagyLupus Erythematosus, SystemicTOR Serine-Threonine KinasesAdultAnimalsAntibody FormationAutoantibodiesB-LymphocytesDisease Models, AnimalFemaleHumansLeukocytes, MononuclearMaleMembrane ProteinsMiceAutoantibodiesMembrane ProteinsMTOR protein, humanTOR Serine-Threonine KinasesAntibodyAutophagyDisease activityPredictive capabilityRheumatoid arthritisSystemic lupus erythematosusTM9SF1

Identifiers

PMID39482663
PMCPMC11526568

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.