Evidence map›Paper›PMID 31293597›Full record

ArticleFrontiers in immunology2019

Granzyme A Stimulates pDCs to Promote Adaptive Immunity via Induction of Type I IFN.

Kanako Shimizu, Satoru Yamasaki, Maki Sakurai, Noriko Yumoto, Mariko Ikeda, Chiemi Mishima-Tsumagari, Mutsuko Kukimoto-Niino, Takashi Watanabe, Masami Kawamura, Mikako Shirouzu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  10. Identification ofBreast cancer (Dove Medical Press) · 2023
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  15. Article
  16. Review
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  18. Article
  19. Granzyme A Produced by γFrontiers in immunology · 2021
    Article
  20. 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

11 authors at 2 institutions in 1 country.

Kanako ShimizuLaboratory for Immunotherapy, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Satoru YamasakiLaboratory for Immunotherapy, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Maki SakuraiLaboratory for Immunotherapy, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Noriko YumotoLaboratory for Immunotherapy, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Mariko IkedaLaboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research, Yokohama, Japan.
Chiemi Mishima-TsumagariLaboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research, Yokohama, Japan.
Mutsuko Kukimoto-NiinoLaboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research, Yokohama, Japan.
Takashi WatanabeLaboratory for Integrative Genomics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Masami KawamuraLaboratory for Immunotherapy, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Mikako ShirouzuLaboratory for Protein Functional and Structural Biology, RIKEN Center for Biosystems Dynamics Research, Yokohama, Japan.
Shin-Ichiro FujiiLaboratory for Immunotherapy, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
RIKEN Center for Integrative Medical Sciences · JPRIKEN Center for Biosystems Dynamics Research · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Granzyme A (GzmA), together with perforin, are well-known for their cytotoxic activity against tumor or virus-infected cells. In addition to this cytotoxic function, GzmA stimulates several immune cell types and induces inflammation in the absence of perforin, however, its effect on the dendritic cell (DC) is unknown. In the current study, we showed that recombinant GzmA induced the phenotypic maturation of plasmacytoid DCs (pDCs) and conventional DCs (cDCs), but not their apoptosis. Particularly, GzmA made pDCs more functional, thus leading to production of type I interferon (IFN) via the TLR9-MyD88 pathway. We also demonstrated that GzmA binds TLR9 and co-localizes with it in endosomes. When co-administered with antigen, GzmA acted as a powerful adjuvant for eliciting antigen-specific cytotoxic CD8

Indexed as

AnimalsCD8-Positive T-LymphocytesDendritic CellsGranzymesImmunity, CellularMiceMice, KnockoutMyeloid Differentiation Factor 88Plasma CellsToll-Like Receptor 9granzyme A, mouseGranzymesMyd88 protein, mouseMyeloid Differentiation Factor 88Tlr9 protein, mouseToll-Like Receptor 9adaptive immunityadjuvantanti-tumor effectdendritic cellgranzyme Ainnate immunityTLR9type I IFN

Identifiers

PMID31293597
PMCPMC6606709
OpenAlexW2954834179

What OpenQuestion holds

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LicenceCC BY
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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.