Evidence map›Paper›PMID 28045014›Full record

ArticleNature communications2017

Death receptor 6 contributes to autoimmunity in lupus-prone mice.

Daisuke Fujikura, Masahiro Ikesue, Tsutomu Endo, Satoko Chiba, Hideaki Higashi, Toshimitsu Uede

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. A structural atlas of death domain fold proteins reveals their versatile roles in biology and function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  7. Bioactive borate glass triggers phenotypic changes in adipose stem cells.Journal of materials science. Materials in medicine · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Daisuke FujikuraDivision of Infection and Immunity, Hokkaido University Research Center for Zoonosis Control, North-20, West-10, Kita-ku, Sapporo 001-0020, Japan.
Masahiro IkesueDivision of Molecular Immunology, Hokkaido University Institute for Genetic Medicine, North-15, West-7, Kita-ku, Sapporo 060-0815, Japan.
Tsutomu EndoDivision of Molecular Immunology, Hokkaido University Institute for Genetic Medicine, North-15, West-7, Kita-ku, Sapporo 060-0815, Japan.
Satoko ChibaDivision of Infection and Immunity, Hokkaido University Research Center for Zoonosis Control, North-20, West-10, Kita-ku, Sapporo 001-0020, Japan.
Hideaki HigashiDivision of Infection and Immunity, Hokkaido University Research Center for Zoonosis Control, North-20, West-10, Kita-ku, Sapporo 001-0020, Japan.
Toshimitsu UedeDivision of Molecular Immunology, Hokkaido University Institute for Genetic Medicine, North-15, West-7, Kita-ku, Sapporo 060-0815, Japan.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expansion of autoreactive follicular helper T (Tfh) cells is tightly restricted to prevent induction of autoantibody-dependent immunological diseases, such as systemic lupus erythematosus (SLE). Here we show expression of an orphan immune regulator, death receptor 6 (DR6/TNFRSF21), on a population of Tfh cells that are highly expanded in lupus-like disease progression in mice. Genome-wide screening reveals an interaction between syndecan-1 and DR6 resulting in immunosuppressive functions. Importantly, syndecan-1 is expressed specifically on autoreactive germinal centre (GC) B cells that are critical for maintenance of Tfh cells. Syndecan-1 expression level on GC B cells is associated with Tfh cell expansion and disease progression in lupus-prone mouse strains. In addition, Tfh cell suppression by DR6-specific monoclonal antibody delays disease progression in lupus-prone mice. These findings suggest that the DR6/syndecan-1 axis regulates aberrant GC reactions and could be a therapeutic target for autoimmune diseases such as SLE.

Indexed as

AutoimmunityGenomeAnimalsAntibodies, MonoclonalB-LymphocytesCell ProliferationDisease Models, AnimalDisease ProgressionFemaleGene Expression RegulationGerminal CenterLupus Erythematosus, SystemicMiceMice, Inbred C57BLRabbitsReceptors, Tumor Necrosis FactorAntibodies, MonoclonalReceptors, Tumor Necrosis FactorSdc1 protein, mouseSyndecan-1Tnfrsf21 protein, mouse

Identifiers

PMID28045014
PMCPMC5216082
OpenAlexW2565178293

What OpenQuestion holds

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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.