Evidence map›Paper›PMID 41541655›Full record

ArticleMedComm2026

Regulation and Mechanism of Deleted in Breast Cancer-1 on Dendritic Cell Function in Systemic Lupus Erythematosus.

Ze Xiu Xiao, Rongzhen Liang, Yan Liu, Changyuan Huang, Qiannan Fang, Xiaojiang Hu, Julie Wang, Nancy Olsen, Dehua Wu, Song Guo Zheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in MedComm, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Ze Xiu XiaoDepartment of Anesthesiology Songjiang Hospital affiliated to the Shanghai Jiao Tong University School of Medicine Shanghai China.
Rongzhen LiangDepartment of Immunology the School of Cell and Gene Therapy Songjiang Research Institute Songjiang Hospital affiliated to the Shanghai Jiao Tong University School of Medicine Shanghai China.
Yan LiuDepartment of Clinical Immunology The Third Affiliated Hospital of Sun Yat-Sen University Guangzhou China.
Changyuan HuangThe First Dongguan Affiliated Hospital Guangdong Medical University Dongguan China.
Qiannan FangDepartment of Immunology the School of Cell and Gene Therapy Songjiang Research Institute Songjiang Hospital affiliated to the Shanghai Jiao Tong University School of Medicine Shanghai China.
Xiaojiang HuDepartment of Clinical Immunology The Third Affiliated Hospital of Sun Yat-Sen University Guangzhou China.
Julie WangDepartment of Immunology the School of Cell and Gene Therapy Songjiang Research Institute Songjiang Hospital affiliated to the Shanghai Jiao Tong University School of Medicine Shanghai China.
Nancy OlsenDepartment of Medicine Penn State College of Medicine Hershey Pennsylvania USA.
Dehua WuDepartment of Anesthesiology Songjiang Hospital affiliated to the Shanghai Jiao Tong University School of Medicine Shanghai China.
Song Guo ZhengDepartment of Immunology the School of Cell and Gene Therapy Songjiang Research Institute Songjiang Hospital affiliated to the Shanghai Jiao Tong University School of Medicine Shanghai China.ORCID https://orcid.org/0000-0002-5611-4774

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple organs and involving both innate and adaptive immunity. Dendritic cells (DCs) play a crucial role in linking innate and adaptive immune responses, and therefore they deeply participate in the initiation and development of SLE. Deleted in breast cancer-1 (DBC1) is a negative regulator of deacetylase SIRT1 (the mammalian homolog of silent information regulator 1) and involves in tissue inflammation. Roles of DBC1 in immune cells remain largely unknown, especially in DCs. We here identified that DBC1 is upregulated in activated DCs, and DBC1 deficiency weakened DC maturation while promoting B7-H1 expression. DC conditional knockout of DBC1 ameliorated murine lupus pathology by decreasing autoantibodies, complement C3, plasma cells, and follicular T helper (Tfh) cells, whereas promoting regulatory T-cell development. We further demonstrated that

Indexed as

autoimmune diseasedeleted in breast cancer‐1dendritic cellsSTAT5systemic lupus erythematosus

Identifiers

PMID41541655
PMCPMC12801396

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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.