Evidence map›Paper›PMID 33249782›Full record

Observational studyFEBS open bio2021

Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus.

Yujun Sheng, Jiali Zhang, Keke Li, Hongyan Wang, Wenjun Wang, Leilei Wen, Jinping Gao, Xianfa Tang, Huayang Tang, He Huang and 6 more

RetractedOpen access · goldAbstract readObservational StudyRetracted Publication
In one paragraph

Observational study in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 1 country.

Yujun ShengDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Jiali ZhangDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Keke LiDepartment of Dermatology, China-Japan Friendship Hospital, Beijing, China.
Hongyan WangDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Wenjun WangDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Leilei WenDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Jinping GaoDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Xianfa TangDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Huayang TangDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
He HuangDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Minglong CaiDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Tao YuanDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Lu LiuDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Xiaodong ZhengDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Zhengwei ZhuDepartment of Dermatology, Institute of Dermatology, the First Affiliated Hospital, Anhui Medical University, Hefei, China.
Yong CuiDepartment of Dermatology, China-Japan Friendship Hospital, Beijing, China.ORCID 0000-0003-3476-8563
Anhui Medical University · CNChina-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal activation of T cells and caused by an imbalance in the production and clearance of apoptotic cells. We previously showed that the transcription regulator Bach2 regulated abnormal B-cell activation in SLE. Here, we investigated whether Bach2 was also involved in Th9 cell differentiation in SLE. We found that the proportion of Th9 cells was enhanced in the peripheral blood mononuclear cells (PBMC) of SLE patients. The PBMC and CD4

Indexed as

Basic-Leucine Zipper Transcription FactorsCase-Control StudiesCell DifferentiationFemaleHealthy VolunteersHumansInterferon Regulatory Factor-4Interferon Regulatory FactorsLupus Erythematosus, SystemicMaleT-Lymphocytes, Helper-InducerT-Lymphocyte SubsetsBACH2 protein, humanBasic-Leucine Zipper Transcription FactorsInterferon Regulatory Factor-4Interferon Regulatory FactorsBach2CD4+ T cellsIL-9systemic lupus erythematosusTh9 cells

Identifiers

PMID33249782
PMCPMC7876501
OpenAlexW3109966776

What Socratic 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 Socratic graph.