Evidence map›Paper›PMID 31462647›Full record

ArticleNature communications2019

Modulation of autoimmune pathogenesis by T cell-triggered inflammatory cell death.

Katsuhiro Sasaki, Ai Himeno, Tomoko Nakagawa, Yoshiteru Sasaki, Hiroshi Kiyonari, Kazuhiro Iwai

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Article
  3. Integrative Transcriptomic and Genetic Analysis PrioritizesClinical, cosmetic and investigational dermatology · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. LUBAC: a new player in polyglucosan body disease.Biochemical Society transactions · 2021
    Review
  13. Review
  14. Review
  15. LUBAC-mediated linear ubiquitination: a crucial regulator of immune signaling.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021
    Review
  16. Review
  17. 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

6 authors at 1 institution in 1 country.

Katsuhiro SasakiDepartment of Molecular and Cellular Physiology, Graduate School of Medicine, Kyoto University, Kyoto, 606-8501, Japan.ORCID http://orcid.org/0000-0002-6211-9088
Ai HimenoDepartment of Molecular and Cellular Physiology, Graduate School of Medicine, Kyoto University, Kyoto, 606-8501, Japan.
Tomoko NakagawaDepartment of Molecular and Cellular Physiology, Graduate School of Medicine, Kyoto University, Kyoto, 606-8501, Japan.
Yoshiteru SasakiDepartment of Molecular and Cellular Physiology, Graduate School of Medicine, Kyoto University, Kyoto, 606-8501, Japan.
Hiroshi KiyonariAnimal Resource Development Unit and Genetic Engineering Team, RIKEN Center for Life Science Technologies, 2-2-3 Minatojima Minami-machi, Chuou-ku, Kobe, 650-0047, Japan.
Kazuhiro IwaiDepartment of Molecular and Cellular Physiology, Graduate School of Medicine, Kyoto University, Kyoto, 606-8501, Japan. kiwai@mcp.med.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0001-5620-5951
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cell-mediated autoimmunity encompasses diverse immunopathological outcomes; however, the mechanisms underlying this diversity are largely unknown. Dysfunction of the tripartite linear ubiquitin chain assembly complex (LUBAC) is associated with distinct autonomous immune-related diseases. Cpdm mice lacking Sharpin, an accessory subunit of LUBAC, have innate immune cell-predominant dermatitis triggered by death of LUBAC-compromised keratinocytes. Here we show that specific gene ablation of Sharpin in mouse Treg causes phenotypes mimicking cpdm-like inflammation. Mechanistic analyses find that multiple types of programmed cell death triggered by TNF from tissue-oriented T cells initiate proinflammatory responses to implicate innate immune-mediated pathogenesis in this T cell-mediated inflammation. Moreover, additional disruption of the Hoip locus encoding the catalytic subunit of LUBAC converts cpdm-like dermatitis to T cell-predominant autoimmune lesions; however, innate immune-mediated pathogenesis still remains. These findings show that T cell-mediated killing and sequential autoinflammation are common and crucial for pathogenic diversity during T cell-mediated autoimmune responses.

Indexed as

AnimalsApoptosisAutoimmunityDermatitisImmunity, InnateInflammationKeratinocytesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNerve Tissue ProteinsT-LymphocytesUbiquitinUbiquitin-Protein LigasesNerve Tissue ProteinssharpinUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID31462647
PMCPMC6713751
OpenAlexW2970524526

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.