Evidence map›Paper›PMID 29908067›Full record

ReviewImmunology2018

Effects of type I interferons in malaria.

Ismail Sebina, Ashraful Haque

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Diagnosis of cerebral malaria: Tools to reduceFrontiers in cellular and infection microbiology · 2023
    Review
  9. Review
  10. Review
  11. Brain endothelial STING1 activation byProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Immunosuppression in Malaria: DoPathogens (Basel, Switzerland) · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Ismail SebinaQIMR Berghofer Medical Research Institute, Herston, QLD, Australia.
Ashraful HaqueQIMR Berghofer Medical Research Institute, Herston, QLD, Australia.ORCID 0000-0003-2260-0026
QIMR Berghofer Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons (IFNs) are a family of cytokines with a wide range of biological activities including anti-viral and immune-regulatory functions. Here, we focus on the protozoan parasitic disease malaria, and examine the effects of type I IFN-signalling during Plasmodium infection of humans and experimental mice. Since the 1960s, there have been many studies in this area, but a simple explanation for the role of type I IFN has not emerged. Although epidemiological data are consistent with roles for type I IFN in influencing malaria disease severity, functional proof of this remains sparse in humans. Several different rodent-infective Plasmodium species have been employed in in vivo studies of parasite-sensing, experimental cerebral malaria, lethal malaria, liver-stage infection, and adaptive T-cell and B-cell immunity. A range of different outcomes in these studies suggests a delicately balanced, multi-faceted and highly complex role for type I IFN-signalling in malaria. This is perhaps unsurprising given the multiple parasite-sensing pathways that can trigger type I IFN production, the multiple isoforms of IFN-α/β that can be produced by both immune and non-immune cells, the differential effects of acute versus chronic type I IFN production, the role of low level 'tonic' type I IFN-signalling, and that signalling can occur via homodimeric IFNAR1 or heterodimeric IFNAR1/2 receptors. Nevertheless, the data indicate that type I IFN-signalling controls parasite numbers during liver-stage infection, and depending on host-parasite genetics, can be either detrimental or beneficial to the host during blood-stage infection. Furthermore, type I IFN can promote cytotoxic T lymphocyte immune pathology and hinder CD4

Indexed as

Adaptive ImmunityAnimalsDisease Models, AnimalHumansImmunomodulationInterferon Type ILife Cycle StagesMalariaMalaria, CerebralPlasmodiumSignal TransductionInterferon Type Icytokinesinterferonsmalariamouse modelsparasitology

Identifiers

PMID29908067
PMCPMC6142290
OpenAlexW2807981220

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.