ArticleLife science alliance2023
Lsd1 safeguards T-cell development via suppressing endogenous retroelements and interferon responses.
Miaoran Xia, Bingbing Wang, Wujianan Sun, Dengyu Ji, Hang Zhou, Xuefeng Huang, Minghang Yu, Ziyang Su, Ping Chen, Kun Qu and 1 more
Open access · goldAbstract read
In one paragraphArticle in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 74% of its field
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed, 0 citations in OpenAlex.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
11 authors at 2 institutions in 2 countries.
Miaoran XiaDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0003-4461-359X Bingbing WangDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Wujianan SunDepartment of Oncology, The First Affiliated Hospital of USTC, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Dengyu JiDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Hang ZhouDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Xuefeng HuangDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Minghang YuDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Ziyang SuDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China.
Ping ChenDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China chenping@ccmu.edu.cn.ORCID https://orcid.org/0000-0003-0295-0846 Kun QuDepartment of Oncology, The First Affiliated Hospital of USTC, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China qukun@ustc.edu.cn.ORCID https://orcid.org/0000-0002-5555-8437 Xi WangDepartment of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory for Tumor Invasion and Metastasis, Capital Medical University, Beijing, China xiwang@ccmu.edu.cn.ORCID https://orcid.org/0000-0001-6753-3053 Capital Medical University · CNUniversity of Science and Technology of China · CN
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
The histone demethylase Lsd1 has been shown to play multiple essential roles in mammalian biology. However, its physiological functions in thymocyte development remain elusive. We observed that the specific deletion of Lsd1 in thymocytes caused significant thymic atrophy and reduced peripheral T cell populations with impaired proliferation capacity. Single-cell RNA sequencing combined with strand-specific total RNA-seq and ChIP-seq analysis revealed that ablation of Lsd1 led to the aberrant derepression of endogenous retroelements, which resulted in a viral mimicry state and activated the interferon pathway. Furthermore, the deletion of Lsd1 blocked the programmed sequential down-regulation of CD8 expression at the DP→CD4
Indexed as
InterferonsRetroelementsAnimalsCell DifferentiationMammalsMiceReceptors, Antigen, T-CellThymus GlandInterferonsReceptors, Antigen, T-CellRetroelements
Identifiers
PMID37429639
PMCPMC10345215
OpenAlexW4383872538
What OpenQuestion holds
Textmetadata
LicenceCC BY
Read underepoch 390