Evidence map›Paper›PMID 27872213›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Autocrine Type I IFN Signaling in Dendritic Cells Stimulated with Fungal β-Glucans or Lipopolysaccharide Promotes CD8 T Cell Activation.

Nargess Hassanzadeh-Kiabi, Alberto Yáñez, Ivy Dang, Gislâine A Martins, David M Underhill, Helen S Goodridge

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Article
  3. Activation of Immune and Antiviral Effects byFoods (Basel, Switzerland) · 2023
    Review
  4. Inside-out assembly of viral antigens for the enhanced vaccination.Signal transduction and targeted therapy · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. β-Glucans fromViruses · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Cells · 2019
    Review
  18. Review
  19. Effects ofPeerJ · 2019
    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

6 authors at 1 institution in 1 country.

Nargess Hassanzadeh-KiabiBoard of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Alberto YáñezBoard of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048.ORCID 0000-0002-7719-1963
Ivy DangBoard of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Gislâine A MartinsResearch Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
David M UnderhillResearch Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048.ORCID 0000-0002-2989-658X
Helen S GoodridgeBoard of Governors Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048; helen.goodridge@csmc.edu.
Cedars-Sinai Medical Center · US

Funding

Non-Toll-like receptor innate immune signalingR01AI071116 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI UNDERHILL, DAVID M. · 2008 to 2023
$6.3M
NIAID NIH HHS R01 AI071116
6 · The paper itself

Abstract

Type I IFNs are key mediators of immune defense against viruses and bacteria. Type I IFNs were also previously implicated in protection against fungal infection, but their roles in antifungal immunity have not been thoroughly investigated. A recent study demonstrated that bacterial and fungal β-glucans stimulate IFN-β production by dendritic cells (DCs) following detection by the Dectin-1 receptor, but the effects of β-glucan-induced type I IFNs have not been defined. We investigated whether type I IFNs regulate CD8 T cell activation by fungal β-glucan particle-stimulated DCs. We demonstrate that β-glucan-stimulated DCs induce CD8 T cell proliferation, activation marker (CD44 and CD69) expression, and production of IFN-γ, IL-2, and granzyme B. Moreover, we show that type I IFNs support robust CD8 T cell activation (proliferation and IFN-γ and granzyme B production) by β-glucan-stimulated DCs in vitro and in vivo due to autocrine effects on the DCs. Specifically, type I IFNs promote Ag presentation on MHC I molecules, CD86 and CD40 expression, and the production of IL-12 p70, IL-2, IL-6, and TNF-α by β-glucan-stimulated DCs. We also demonstrate a role for autocrine type I IFN signaling in bacterial LPS-induced DC maturation, although, in the context of LPS stimulation, this mechanism is not so critical for CD8 T cell activation (promotes IFN-γ production but not proliferation or granzyme B production). This study provides insight into the mechanisms underlying CD8 T cell activation during infection, which may be useful in the rational design of vaccines directed against pathogens and tumors.

Indexed as

AnimalsAutocrine Communicationbeta-GlucansBlotting, WesternCD8-Positive T-LymphocytesCoculture TechniquesDendritic CellsFlow CytometryFungal ProteinsInterferon Type ILipopolysaccharidesLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutSignal Transductionbeta-GlucansFungal ProteinsInterferon Type ILipopolysaccharides

Identifiers

PMID27872213
PMCPMC5173402
OpenAlexW2554643856

What OpenQuestion holds

Textmetadata
LicenceTDM
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.