Evidence map›Paper›PMID 27793594›Full record

ArticleImmunity2016

Cross-Regulation of Two Type I Interferon Signaling Pathways in Plasmacytoid Dendritic Cells Controls Anti-malaria Immunity and Host Mortality.

Xiao Yu, Baowei Cai, Mingjun Wang, Peng Tan, Xilai Ding, Jian Wu, Jian Li, Qingtian Li, Pinghua Liu, Changsheng Xing and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

84 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
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  13. cGAS: action in the nucleus.Frontiers in immunology · 2024
    Review
  14. Human transcriptional signature of protection afterHuman vaccines & immunotherapeutics · 2023
    Article
  15. Article
  16. Review
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  19. Article
  20. Article

24 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

13 authors at 5 institutions in 2 countries.

Xiao YuSchool of Life Sciences, Sun Yat-Sen University, 510275 Guangzhou, P.R. China; Center for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Baowei CaiCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361005 Fujian, P.R. China.
Mingjun WangZhongshan School of Medicine, Sun Yat-Sen University, 510275 Guangzhou, P.R. China; Center for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Peng TanCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA; Institute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, TX 77030, USA.
Xilai DingCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Jian WuLaboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Jian LiState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361005 Fujian, P.R. China.
Qingtian LiCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Pinghua LiuCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Changsheng XingCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Helen Y WangCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA.
Xin-Zhuan SuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, 361005 Fujian, P.R. China; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: xsu@niaid.nih.gov.
Rong-Fu WangCenter for Inflammation and Epigenetics, Houston Methodist Research Institute, Houston, TX 77030, USA; Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY 10065, USA; Institute of Biosciences and Technology, College of Medicine, Texas A&M University, Houston, TX 77030, USA. Electronic address: rwang3@houstonmethodist.org.
Houston Methodist · USSun Yat-sen University · CNXiamen University · CNNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Malaria Parasite Sexual Development, Drug Resistance, and EvolutionZIAAI000892 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, XINZHUAN · 2009 to 2025
$23.3M
Novel Strategies for Intervention of Inflammatory Diseases and Cancer - Research Supplement to R01-CA101795R01CA101795 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WANG, RONGFU · 2004 to 2022
$4.6M
Development of Novel Vaccines for Cocaine AbuseR01DA030338 · NIDA · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ORSON, FRANK M, WANG, RONGFU · 2010 to 2014
$1.6M
NCI NIH HHS R01 CA101795NIDA NIH HHS R01 DA030338
6 · The paper itself

Abstract

Type I interferon (IFN) is critical for controlling pathogen infection; however, its regulatory mechanisms in plasmacytoid cells (pDCs) still remain unclear. Here, we have shown that nucleic acid sensors cGAS-, STING-, MDA5-, MAVS-, or transcription factor IRF3-deficient mice produced high amounts of type I IFN-α and IFN-β (IFN-α/β) in the serum and were resistant to lethal plasmodium yoelii YM infection. Robust IFN-α/β production was abolished when gene encoding nucleic acid sensor TLR7, signaling adaptor MyD88, or transcription factor IRF7 was ablated or pDCs were depleted. Further, we identified SOCS1 as a key negative regulator to inhibit MyD88-dependent type I IFN signaling in pDCs. Finally, we have demonstrated that pDCs, cDCs, and macrophages were required for generating IFN-α/β-induced subsequent protective immunity. Thus, our findings have identified a critical regulatory mechanism of type I IFN signaling in pDCs and stage-specific function of immune cells in generating potent immunity against lethal YM infection.

Indexed as

Adaptive ImmunityAnimalsDendritic CellsDisease Models, AnimalEnzyme-Linked Immunosorbent AssayGene Knockdown TechniquesInterferon Type IMalariaMiceMice, KnockoutPlasmodium yoeliiPolymerase Chain ReactionSignal TransductionInterferon Type IInnate immune responseMalaria infectionPlasmacytoid dendritic cellsType I IFN signaling

Identifiers

PMID27793594
PMCPMC7128466
OpenAlexW2538848459

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.