Evidence map›Paper›PMID 32572241›Full record

ArticleNature immunology2020

Tet2 and Tet3 in B cells are required to repress CD86 and prevent autoimmunity.

Shinya Tanaka, Wataru Ise, Takeshi Inoue, Ayako Ito, Chisato Ono, Yoshihito Shima, Shuhei Sakakibara, Manabu Nakayama, Kentaro Fujii, Ikuo Miura and 15 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.1field-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

58 citing papers in PubMed, 91 citations in OpenAlex.

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  18. Methylation of T and B Lymphocytes in Autoimmune Rheumatic Diseases.Clinical reviews in allergy & immunology · 2024
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 10 institutions in 2 countries.

Shinya TanakaLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
Wataru IseLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
Takeshi InoueLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
Ayako ItoLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
Chisato OnoDivision of Immunology and Genome Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Yoshihito ShimaLaboratory of Thermo-Therapeutics for Vascular Dysfunction, Osaka University, Suita, Japan.
Shuhei SakakibaraLaboratory of Immune Regulation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.ORCID http://orcid.org/0000-0003-3157-5870
Manabu NakayamaLaboratory of Medical Omics Research, Kazusa DNA Research Institute, Kisarazu, Japan.
Kentaro FujiiLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
Ikuo MiuraTechnology and Development Team for Mouse Phenotype Analysis, RIKEN BioResource Research Center, Tsukuba, Japan.
Jafar SharifLaboratory of Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Haruhiko KosekiLaboratory of Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Pandelakis A KoniGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Indu RamanMicroarray Core Facility, Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Quan-Zhen LiMicroarray Core Facility, Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Masato KuboDivision of Molecular Pathology, Research Institute for Biomedical Science, Tokyo University of Science, Noda, Japan.
Katsunori FujikiInstitute of Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.
Ryuichiro NakatoInstitute of Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-3019-5817
Katsuhiko ShirahigeInstitute of Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.
Hiromitsu ArakiDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Fumihito MiuraDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID http://orcid.org/0000-0003-2656-486X
Takashi ItoDepartment of Biochemistry, Kyushu University Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.ORCID http://orcid.org/0000-0001-6097-2803
Eiryo KawakamiMedical Sciences Innovation Hub Program, RIKEN, Yokohama, Japan.
Yoshihiro BabaLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan. babay@bioreg.kyushu-u.ac.jp.ORCID http://orcid.org/0000-0001-7753-0905
Tomohiro KurosakiLaboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Japan. kurosaki@ifrec.osaka-u.ac.jp.ORCID http://orcid.org/0000-0002-6352-304X
Kyushu University · JPThe University of Osaka · JPThe University of Tokyo · JPChiba University · JPRIKEN Center for Integrative Medical Sciences · JPThe University of Texas Southwestern Medical Center · USAugusta University Health · USKazusa DNA Research Institute · JPRIKEN BioResource Research Center · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A contribution of epigenetic modifications to B cell tolerance has been proposed but not directly tested. Here we report that deficiency of ten-eleven translocation (Tet) DNA demethylase family members Tet2 and Tet3 in B cells led to hyperactivation of B and T cells, autoantibody production and lupus-like disease in mice. Mechanistically, in the absence of Tet2 and Tet3, downregulation of CD86, which normally occurs following chronic exposure of self-reactive B cells to self-antigen, did not take place. The importance of dysregulated CD86 expression in Tet2- and Tet3-deficient B cells was further demonstrated by the restriction, albeit not complete, on aberrant T and B cell activation following anti-CD86 blockade. Tet2- and Tet3-deficient B cells had decreased accumulation of histone deacetylase 1 (HDAC1) and HDAC2 at the Cd86 locus. Thus, our findings suggest that Tet2- and Tet3-mediated chromatin modification participates in repression of CD86 on chronically stimulated self-reactive B cells, which contributes, at least in part, to preventing autoimmunity.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityB7-2 AntigenB-LymphocytesDioxygenasesDNA-Binding ProteinsEpigenesis, GeneticLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicProto-Oncogene ProteinsB7-2 AntigenCd86 protein, mouseDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsTet2 protein, mouseTet3 protein, mouse

Identifiers

PMID32572241
OpenAlexW3036830466

What OpenQuestion holds

Textmetadata
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.