Evidence map›Paper›PMID 22315415›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Plasmacytoid dendritic cells control T-cell response to chronic viral infection.

Luisa Cervantes-Barragan, Kanako L Lewis, Sonja Firner, Volker Thiel, Stephanie Hugues, Walter Reith, Burkhard Ludewig, Boris Reizis

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

136 citing papers in PubMed, 207 citations in OpenAlex.

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  17. Human CD34Cellular and molecular life sciences : CMLS · 2023
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76 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 2 countries.

Luisa Cervantes-BarraganInstitute of Immunobiology, Kantonal Hospital St Gallen, CH-9007 St Gallen, Switzerland.
Kanako L Lewis
Sonja Firner
Volker Thiel
Stephanie Hugues
Walter Reith
Burkhard Ludewig
Boris Reizis
Kantonsspital St. Gallen · CHColumbia University Irving Medical Center · USUniversity of Geneva · CH

Funding

Molecular Control of Plasmacytoid Dendritic Cell Development and FunctionR37AI072571 · NIAID · UNIVERSITY OF CHICAGO · PI Boris Reizis · 2018 to 2026
$5.3M
Molecular Control of Plasmacytoid Dendritic Cell Development and FunctionR01AI072571 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI REIZIS, BORIS · 2008 to 2017
$4.1M
TRAINING PROGRAM IN MICROBIOLOGY FOR INFECTIOUS DISEASEST32AI007161 · NIAID · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI FIDOCK, DAVID A · 1985 to 2008
$1.9M
Genetic Approaches to the Study of Plasmacytoid Dendritic Cell FunctionR21AI085439 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REIZIS, BORIS · 2010 to 2011
$432k
NIAID NIH HHS AI007161NIAID NIH HHS AI072571NIAID NIH HHS AI085439NIAID NIH HHS R01 AI072571NIAID NIH HHS R21 AI085439NIAID NIH HHS R37 AI072571NIAID NIH HHS T32 AI007161
6 · The paper itself

Abstract

Infections with persistent viruses are a frequent cause of immunosuppression, autoimmune sequelae, and/or neoplastic disease. Plasmacytoid dendritic cells (pDCs) are innate immune cells that produce type I interferon (IFN-I) and other cytokines in response to virus-derived nucleic acids. Persistent viruses often cause depletion or functional impairment of pDCs, but the role of pDCs in the control of these viruses remains unclear. We used conditional targeting of pDC-specific transcription factor E2-2 to generate mice that constitutively lack pDCs in peripheral lymphoid organs and tissues. The profound impact of pDC deficiency on innate antiviral responses was revealed by the failure to control acute infection with the cytopathic mouse hepatitis virus. Furthermore, pDC-deficient animals failed to clear lymphocytic choriomeningitis virus (LCMV) from hematopoietic organs during persistent LCMV infection. This failure was associated with reduced numbers and functionality of LCMV-specific CD4(+) helper T cells and impaired antiviral CD8(+) T-cell responses. Adoptive transfer of LCMV-specific T cells revealed that both CD4(+) and CD8(+) T cells required IFN-I for expansion, but only CD4(+) T cells required the presence of pDCs. In contrast, mice with pDC-specific loss of MHC class II expression supported normal CD4(+) T-cell response to LCMV. These data suggest that pDCs facilitate CD4(+) helper T-cell responses to persistent viruses independently of direct antigen presentation. Thus pDCs provide an essential link between innate and adaptive immunity to chronic viral infection, likely through the secretion of IFN-I and other cytokines.

Indexed as

AnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsChronic DiseaseCoronavirus InfectionsDendritic CellsDisease Models, AnimalGene TargetingLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMurine hepatitis virusT-LymphocytesTranscription Factor 4Virus DiseasesBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsTcf4 protein, mouseTranscription Factor 4

Identifiers

PMID22315415
PMCPMC3286988
OpenAlexW2029629696

What OpenQuestion holds

Textmetadata
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.