Evidence map›Paper›PMID 24789914›Full record

ArticleThe Journal of clinical investigation2014

Type I IFN signaling in CD8- DCs impairs Th1-dependent malaria immunity.

Ashraful Haque, Shannon E Best, Marcela Montes de Oca, Kylie R James, Anne Ammerdorffer, Chelsea L Edwards, Fabian de Labastida Rivera, Fiona H Amante, Patrick T Bunn, Meru Sheel and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 121 citations in OpenAlex.

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12 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

21 authors at 7 institutions in 4 countries.

Ashraful Haque
Shannon E Best
Marcela Montes de Oca
Kylie R James
Anne Ammerdorffer
Chelsea L Edwards
Fabian de Labastida Rivera
Fiona H Amante
Patrick T Bunn
Meru Sheel
Ismail Sebina
Motoko Koyama
Antiopi Varelias
Paul J Hertzog
Ulrich Kalinke
Sin Yee Gun
Laurent Rénia
Christiane Ruedl
Kelli P A MacDonald
Geoffrey R Hill
Christian R Engwerda
QIMR Berghofer Medical Research Institute · AUNational Institute of Malaria Research · INThe University of Queensland · AUAgency for Science, Technology and Research · SGCenter for Experimental and Clinical Infection Research · DEMonash Institute of Medical Research · AUNanyang Technological University · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many pathogens, including viruses, bacteria, and protozoan parasites, suppress cellular immune responses through activation of type I IFN signaling. Recent evidence suggests that immune suppression and susceptibility to the malaria parasite, Plasmodium, is mediated by type I IFN; however, it is unclear how type I IFN suppresses immunity to blood-stage Plasmodium parasites. During experimental severe malaria, CD4+ Th cell responses are suppressed, and conventional DC (cDC) function is curtailed through unknown mechanisms. Here, we tested the hypothesis that type I IFN signaling directly impairs cDC function during Plasmodium infection in mice. Using cDC-specific IFNAR1-deficient mice, and mixed BM chimeras, we found that type I IFN signaling directly affects cDC function, limiting the ability of cDCs to prime IFN-γ-producing Th1 cells. Although type I IFN signaling modulated all subsets of splenic cDCs, CD8- cDCs were especially susceptible, exhibiting reduced phagocytic and Th1-promoting properties in response to type I IFNs. Additionally, rapid and systemic IFN-α production in response to Plasmodium infection required type I IFN signaling in cDCs themselves, revealing their contribution to a feed-forward cytokine-signaling loop. Together, these data suggest abrogation of type I IFN signaling in CD8- splenic cDCs as an approach for enhancing Th1 responses against Plasmodium and other type I IFN-inducing pathogens.

Indexed as

AnimalsCD8 AntigensDendritic CellsFemaleImmune ToleranceImmunity, CellularInterferon Type IMalariaMiceMice, Inbred C57BLMice, KnockoutMonocytesPlasmodium bergheiReceptor, Interferon alpha-betaSignal TransductionTh1 CellsCD8 AntigensIfnar1 protein, mouseInterferon Type IReceptor, Interferon alpha-beta

Identifiers

PMID24789914
PMCPMC4038565
OpenAlexW2164889791

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.