Evidence map›Paper›PMID 24042114›Full record

ArticleInfection and immunity2013

Toll-like receptor 7 mediates early innate immune responses to malaria.

Alyssa Baccarella, Mary F Fontana, Eunice C Chen, Charles C Kim

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.2field-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

45 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. eLife · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. The NF-κB Pathway: Modulation byFrontiers in cellular and infection microbiology · 2021
    Review
  11. Roles of TLR7 inFrontiers in cellular and infection microbiology · 2021
    Article
  12. RTP4 inhibits IFN-I response and enhances experimental cerebral malaria and neuropathology.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Article
  14. Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Frontiers in immunology · 2019
    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

4 authors at 1 institution in 1 country.

Alyssa BaccarellaDivision of Experimental Medicine, Department of Medicine, University of California, San Francisco, California, USA.
Mary F Fontana
Eunice C Chen
Charles C Kim
University of California, San Francisco · US

Funding

MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
Microbial Pathogenesis and Host DefenseT32AI060537 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joanne N. Engel · 2004 to 2026
$6.5M
Immunological detection and control of experimental uncomplicated malariaR00AI085035 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KIM, CHARLES C · 2011 to 2012
$492k
Immunological detection and control of experimental uncomplicated malariaK99AI085035 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KIM, CHARLES C · 2010 to 2010
$88k
NIAID NIH HHS K99 AI085035NIAID NIH HHS R00 AI085035NIAID NIH HHS T32 AI007334NIAID NIH HHS T32 AI060537
6 · The paper itself

Abstract

Innate immune recognition of malaria parasites is the critical first step in the development of the host response. At present, Toll-like receptor 9 (TLR9) is thought to play a central role in sensing malaria infection. However, we and others have observed that Tlr9(-/-) mice, in contrast to mice deficient in the downstream adaptor, Myeloid differentiation primary response gene 88 (MYD88), exhibit few deficiencies in immune function during early infection with the malaria parasite Plasmodium chabaudi, implying that another MYD88-dependent receptor also contributes to the antimalarial response. Here we use candidate-based screening to identify TLR7 as a key sensor of early P. chabaudi infection. We show that TLR7 mediates a rapid systemic response to infection through induction of cytokines such as type I interferons (IFN-I), interleukin 12, and gamma interferon. TLR7 is also required for induction of IFN-I by other species and strains of Plasmodium, including an etiological agent of human disease, P. falciparum, suggesting that malaria parasites harbor a common pathogen-associated molecular pattern (PAMP) recognized by TLR7. In contrast to the nonredundant requirement for TLR7 in early immune activation, sensing through both TLR7 and TLR9 was required for proinflammatory cytokine production and immune cell activation during the peak of parasitemia. Our findings indicate that TLR7 plays a central role in early immune activation during malaria infection, whereas TLR7 and TLR9 contribute combinatorially to immune responses as infection progresses.

Indexed as

AnimalsImmunity, InnateInterferon-gammaInterferon Type IInterleukin-12MalariaMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88ParasitemiaPlasmodium chabaudiToll-Like Receptor 7Toll-Like Receptor 9Interferon-gammaInterferon Type IInterleukin-12Membrane GlycoproteinsMyd88 protein, mouseMyeloid Differentiation Factor 88Tlr7 protein, mouseTlr9 protein, mouseToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID24042114
PMCPMC3837989
OpenAlexW2145182918

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.