Evidence map›Paper›PMID 26773151›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

CD28 Deficiency Enhances Type I IFN Production by Murine Plasmacytoid Dendritic Cells.

Monica Macal, Miguel A Tam, Charles Hesser, Jeremy Di Domizio, Psylvia Leger, Michel Gilliet, Elina I Zuniga

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Type I Interferon Production of Plasmacytoid Dendritic Cells under Control.International journal of molecular sciences · 2021
    Review
  3. The Role of Cutaneous Type I IFNs in Autoimmune and Autoinflammatory Diseases.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Review
  4. Article
  5. Infection and cancer suppress pDC derived IFN-I.Current opinion in immunology · 2020
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

7 authors at 2 institutions in 2 countries.

Monica MacalDivision of Biological Sciences, University of California San Diego, La Jolla, CA 92093; and.
Miguel A TamDivision of Biological Sciences, University of California San Diego, La Jolla, CA 92093; and.ORCID http://orcid.org/0000-0001-8094-7090
Charles HesserDivision of Biological Sciences, University of California San Diego, La Jolla, CA 92093; and.ORCID http://orcid.org/0000-0002-6690-3283
Jeremy Di DomizioService de Dermatologie et vénéréologie, Centre Hospitalier Universitaire Vaudois, University Hospital of Lausanne, Lausanne CH-1011, Switzerland.ORCID http://orcid.org/0000-0002-6281-3918
Psylvia LegerDivision of Biological Sciences, University of California San Diego, La Jolla, CA 92093; and.
Michel GillietService de Dermatologie et vénéréologie, Centre Hospitalier Universitaire Vaudois, University Hospital of Lausanne, Lausanne CH-1011, Switzerland.
Elina I ZunigaDivision of Biological Sciences, University of California San Diego, La Jolla, CA 92093; and eizuniga@ucsd.edu.
University of California San Diego · USUniversity Hospital of Lausanne · CH

Funding

Inhibitory Pathways Underlying Viral Persistence In VivoR01AI081923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Elina I Zuniga · 2009 to 2026
$6.6M
Positive Immune-regulators During Chronic Viral InfectionsR01AI113923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZUNIGA, ELINA I · 2015 to 2024
$5.1M
NIAID NIH HHS R01 AI081923NIAID NIH HHS R01 AI113923PHS HHS A1081923
6 · The paper itself

Abstract

Type I IFNs (IFN-I) are key innate mediators that create a profound antiviral state and orchestrate the activation of almost all immune cells. Plasmacytoid dendritic cells (pDCs) are the most powerful IFN-I-producing cells and play important roles during viral infections, cancer, and autoimmune diseases. By comparing gene expression profiles of murine pDCs and conventional DCs, we found that CD28, a prototypic T cell stimulatory receptor, was highly expressed in pDCs. Strikingly, CD28 acted as a negative regulator of pDC IFN-I production upon TLR stimulation but did not affect pDC survival or maturation. Importantly, cell-intrinsic CD28 expression restrained pDC (and systemic) IFN-I production during in vivo RNA and DNA viral infections, limiting antiviral responses and enhancing viral growth early after exposure. Finally, CD28 also downregulated IFN-I response upon skin injury. Our study identified a new pDC regulatory mechanism by which the same CD28 molecule that promotes stimulation in most cells that express it is co-opted to negatively regulate pDC IFN-I production and limit innate responses.

Indexed as

AnimalsCD28 AntigensDendritic CellsEnzyme-Linked Immunosorbent AssayFlow CytometryHumansInterferon Type IMiceMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisReal-Time Polymerase Chain ReactionTranscriptomeCD28 AntigensInterferon Type I

Identifiers

PMID26773151
PMCPMC4744517
OpenAlexW2253738666

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.