Evidence map›Paper›PMID 24474774›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells.

Qingfeng Chen, Anburaj Amaladoss, Weijian Ye, Min Liu, Sara Dummler, Fang Kong, Lan Hiong Wong, Hooi Linn Loo, Eva Loh, Shu Qi Tan and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 81 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Review
  9. Natural killer cell antibody-dependent cellular cytotoxicity toClinical & translational immunology · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Host-parasite interactions duringFrontiers in immunology · 2022
    Review
  15. Vaccines · 2021
    Review
  16. Role of Heat Shock Proteins in Immune Modulation in Malaria.Advances in experimental medicine and biology · 2021
    Article
  17. Review
  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

16 authors at 6 institutions in 2 countries.

Qingfeng ChenInterdisciplinary Research Group in Infectious Diseases, Singapore-MIT Alliance for Research and Technology, Singapore 138602.
Anburaj Amaladoss
Weijian Ye
Min Liu
Sara Dummler
Fang Kong
Lan Hiong Wong
Hooi Linn Loo
Eva Loh
Shu Qi Tan
Thiam Chye Tan
Kenneth T E Chang
Ming Dao
Subra Suresh
Peter R Preiser
Jianzhu Chen
Singapore-MIT Alliance for Research and Technology · SGKK Women's and Children's Hospital · SGNanyang Technological University · SGCarnegie Mellon University · USMassachusetts Institute of Technology · USNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunodeficient mouse-human chimeras provide a powerful approach to study host-specific pathogens, such as Plasmodium falciparum that causes human malaria. Supplementation of immunodeficient mice with human RBCs supports infection by human Plasmodium parasites, but these mice lack the human immune system. By combining human RBC supplementation and humanized mice that are optimized for human immune cell reconstitution, we have developed RBC-supplemented, immune cell-optimized humanized (RICH) mice that support multiple cycles of P. falciparum infection. Depletion of human natural killer (NK) cells, but not macrophages, in RICH mice results in a significant increase in parasitemia. Further studies in vitro show that NK cells preferentially interact with infected RBCs (iRBCs), resulting in the activation of NK cells and the elimination of iRBCs in a contact-dependent manner. We show that the adhesion molecule lymphocyte-associated antigen 1 is required for NK cell interaction with and elimination of iRBCs. Development of RICH mice and validation of P. falciparum infection should facilitate the dissection of human immune responses to malaria parasite infection and the evaluation of therapeutics and vaccines.

Indexed as

AnimalsCell AdhesionErythrocytesHumansKiller Cells, NaturalMalaria, FalciparumMiceParasitemiaPlasmodium falciparumhumanized mouse modelLFA-1malaria infectionNK killing

Identifiers

PMID24474774
PMCPMC3910619
OpenAlexW2125951290

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.