Evidence map›Paper›PMID 38291338›Full record

ArticleEMBO reports2024

A lncRNA Dleu2-encoded peptide relieves autoimmunity by facilitating Smad3-mediated Treg induction.

Sibei Tang, Junxun Zhang, Fangzhou Lou, Hong Zhou, Xiaojie Cai, Zhikai Wang, Libo Sun, Yang Sun, Xiangxiao Li, Li Fan and 7 more

Open access · diamondAbstract read
In one paragraph

Article in EMBO reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

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  20. Noncanonical microprotein regulation of immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
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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

17 authors at 1 institution in 1 country.

Sibei Tang *Precision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Junxun Zhang *Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Fangzhou LouPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Hong ZhouPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.ORCID 0000-0003-0586-525X
Xiaojie CaiPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.ORCID 0000-0001-7297-4865
Zhikai WangShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Libo SunPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.ORCID 0000-0002-3805-5870
Yang SunPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Xiangxiao LiPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Li FanPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Yan LiPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Xinping JinShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Siyu DengPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Qianqian YinShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Jing BaiPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China.
Hong WangShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Honglin WangPrecision Research Center for Refractory Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201610, China. honglin.wang@sjtu.edu.cn.ORCID 0000-0001-6302-6927
Shanghai Jiao Tong University · CN

Funding

Clinical Research Plan of Shanghai Shenkang Hospital Development Center SHDC2020CR3061BExperimental Animal Research Project of "Sientific and Technological Innovation Action Plan" 22140903100Integrated innovation fund of Shanghai Jiao Tong University 2021JCPT04MOST | National Key Research and Development Program of the Ministry of Science and Technology 2020YFA0112900MOST | National Natural Science Foundation of China (NSFC) 81930088MOST | National Natural Science Foundation of China (NSFC) 82070509MOST | National Natural Science Foundation of China (NSFC) 82073428MOST | National Natural Science Foundation of China (NSFC) 82101909MOST | National Natural Science Foundation of China (NSFC) 82103719National Natural Science Foundation of China Original Exploration Program 82050009Shanghai Action Plan for Science, Technology and Innovation 22QA1407600Shanghai Action Plan for Science, Technology and Innovation 23ZR1480700SJTU Trans-med Awards Research 20210102
6 · The paper itself

Abstract

Micropeptides encoded by short open reading frames (sORFs) within long noncoding RNAs (lncRNAs) are beginning to be discovered and characterized as regulators of biological and pathological processes. Here, we find that lncRNA Dleu2 encodes a 17-amino-acid micropeptide, which we name Dleu2-17aa, that is abundantly expressed in T cells. Dleu2-17aa promotes inducible regulatory T (iTreg) cell generation by interacting with SMAD Family Member 3 (Smad3) and enhancing its binding to the Foxp3 conserved non-coding DNA sequence 1 (CNS1) region. Importantly, the genetic deletion of Dleu2-17aa in mice by start codon mutation impairs iTreg generation and worsens experimental autoimmune encephalomyelitis (EAE). Conversely, the exogenous supplementation of Dleu2-17aa relieves EAE. Our findings demonstrate an indispensable role of Dleu2-17aa in maintaining immune homeostasis and suggest therapeutic applications for this peptide in treating autoimmune diseases.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalRNA, Long NoncodingAnimalsAutoimmunityMicePeptidesSmad3 ProteinT-Lymphocytes, RegulatoryTransferasesDleu2 protein, mousePeptidesRNA, Long NoncodingSmad3 ProteinSmad3 protein, mouseTransferasesAutoimmunityDleu2LncRNA Encoded MicropeptideSmad3Treg Cell

Identifiers

PMID38291338
PMCPMC10933344
OpenAlexW4391338525

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.