Evidence map›Paper›PMID 29669251›Full record

ArticleImmunity2018

Self-Renewal and Toll-like Receptor Signaling Sustain Exhausted Plasmacytoid Dendritic Cells during Chronic Viral Infection.

Monica Macal, Yeara Jo, Simone Dallari, Aaron Y Chang, Jihong Dai, Shobha Swaminathan, Ellen J Wehrens, Patricia Fitzgerald-Bocarsly, Elina I Zúñiga

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

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  12. A type I interferon regulatory network for human plasmacytoid dendritic cells based on heparin, membrane-bound and soluble BDCA-2.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

9 authors at 2 institutions in 1 country.

Monica MacalDivision of Biological Sciences, University of California San Diego, La Jolla, San Diego, CA 92093, USA.
Yeara JoDivision of Biological Sciences, University of California San Diego, La Jolla, San Diego, CA 92093, USA.
Simone DallariDivision of Biological Sciences, University of California San Diego, La Jolla, San Diego, CA 92093, USA.
Aaron Y ChangDivision of Biological Sciences, University of California San Diego, La Jolla, San Diego, CA 92093, USA.
Jihong DaiDepartment of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103, USA.
Shobha SwaminathanDepartment of Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103, USA.
Ellen J WehrensDivision of Biological Sciences, University of California San Diego, La Jolla, San Diego, CA 92093, USA.
Patricia Fitzgerald-BocarslyDepartment of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103, USA.
Elina I ZúñigaDivision of Biological Sciences, University of California San Diego, La Jolla, San Diego, CA 92093, USA. Electronic address: eizuniga@ucsd.edu.
University of California San Diego · USRutgers, The State University of New Jersey · US

Funding

VirologyP30AI036214 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Maile Ann Young Karris · 1994 to 2026
$78.4M
Inhibitory Pathways Underlying Viral Persistence In VivoR01AI081923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Elina I Zuniga · 2009 to 2026
$6.6M
ROLE OF INTERFERON-ALPHA IN AIDS PATHOGENESISR01AI026806 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI FITZGERALD-BOCARSLY, PATRICIA · 1991 to 2014
$6.0M
Positive Immune-regulators During Chronic Viral InfectionsR01AI113923 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZUNIGA, ELINA I · 2015 to 2024
$5.1M
Contribution of plasmacytoid DCs to immune senescence in HIV infectionR01AI106125 · NIAID · RBHS-NEW JERSEY MEDICAL SCHOOL · PI FITZGERALD-BOCARSLY, PATRICIA · 2014 to 2017
$1.6M
NIAID NIH HHS P30 AI036214NIAID NIH HHS R01 AI026806NIAID NIH HHS R01 AI081923NIAID NIH HHS R01 AI106125NIAID NIH HHS R01 AI113923
6 · The paper itself

Abstract

Although characterization of T cell exhaustion has unlocked powerful immunotherapies, the mechanisms sustaining adaptations of short-lived innate cells to chronic inflammatory settings remain unknown. During murine chronic viral infection, we found that concerted events in bone marrow and spleen mediated by type I interferon (IFN-I) and Toll-like receptor 7 (TLR7) maintained a pool of functionally exhausted plasmacytoid dendritic cells (pDCs). In the bone marrow, IFN-I compromised the number and the developmental capacity of pDC progenitors, which generated dysfunctional pDCs. Concurrently, exhausted pDCs in the periphery were maintained by self-renewal via IFN-I- and TLR7-induced proliferation of CD4

Indexed as

3T3 CellsAnimalsCarrier ProteinsCell LineCell ProliferationCell Self RenewalDendritic CellsDNA-Binding ProteinsHumansInflammationInterferon Type ILymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMembrane GlycoproteinsMiceMice, Inbred C57BLBcl11a protein, mouseCarrier ProteinsDNA-Binding ProteinsInterferon Type IMembrane GlycoproteinsNuclear ProteinsRepressor ProteinsSPIB protein, humanTcf4 protein, mouseTlr7 protein, mouseToll-Like Receptor 7Transcription Factor 4Transcription Factorscancerchronic viral infectionexhaustionHIVLCMVplasmacytoid dendritic cellsTLRtype I interferon

Identifiers

PMID29669251
PMCPMC5937984
OpenAlexW2802753517

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.