Evidence map›Paper›PMID 17923502›Full record

ArticleThe Journal of experimental medicine2007

TAP-1 indirectly regulates CD4+ T cell priming in Toxoplasma gondii infection by controlling NK cell IFN-gamma production.

Romina S Goldszmid, Andre Bafica, Dragana Jankovic, Carl G Feng, Pat Caspar, Robin Winkler-Pickett, Giorgio Trinchieri, Alan Sher

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. Vaccines · 2024
    Article
  4. Article
  5. Review
  6. Review
  7. Innate Lymphoid Cells in Response to Intracellular Pathogens: ProtectionFrontiers in cellular and infection microbiology · 2021
    Review
  8. Article
  9. NK Cells Negatively Regulate CD8 T Cells to Promote Immune Exhaustion and ChronicFrontiers in cellular and infection microbiology · 2020
    Article
  10. Article
  11. Review
  12. eLife · 2019
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Conventional CD4Nature communications · 2017
    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

8 authors at 3 institutions in 2 countries.

Romina S GoldszmidImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD 20892, USA. rgoldszmid@niaid.nih.gov
Andre Bafica
Dragana Jankovic
Carl G Feng
Pat Caspar
Robin Winkler-Pickett
Giorgio Trinchieri
Alan Sher
National Institutes of Health · USNational Cancer Institute · USNational Institute of Allergy and Infectious Diseases · US

Funding

Immune Regulation In Toxoplasmosis And Other Opportunistic InfectionsZIAAI000579 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2009 to 2022
$7.8M
STUDIES ON IMMUNE REGULATION IN TOXOPLASMOSISZ01AI000579 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI SHER, ALAN · 1990 to 2008
$4.0M
Intramural NIH HHS
6 · The paper itself

Abstract

To investigate if transporter associated with antigen processing (TAP)-1 is required for CD8(+) T cell-mediated control of Toxoplasma gondii in vivo, we compared the resistance of TAP-1(-/-), CD8(-/-), and wild-type (WT) mice to infection with the parasite. Unexpectedly, TAP-1(-/-) mice displayed greater susceptibility than CD8(-/-), beta(2)-microglobulin(-/-) (beta(2)m(-/-)), or WT mice to infection with an avirulent parasite strain. The decreased resistance of the TAP-1(-/-) mice correlated with a reduction in the frequency of activated (CD62L(low) CD44(hi)) and interferon (IFN)-gamma-producing CD4(+) T cells. Interestingly, infected TAP-1(-/-) mice also showed reduced numbers of IFN-gamma-producing natural killer (NK) cells relative to WT, CD8(-/-), or beta(2)m(-/-) mice, and after NK cell depletion both CD8(-/-) and WT mice succumbed to infection with the same kinetics as TAP-1(-/-) animals and displayed impaired CD4(+) T cell IFN-gamma responses. Moreover, adoptive transfer of NK cells obtained from IFN-gamma(+/+), but not IFN-gamma(-/-), animals restored the CD4(+) T cell response of infected TAP-1(-/-) mice to normal levels. These results reveal a role for TAP-1 in the induction of IFN-gamma-producing NK cells and demonstrate that NK cell licensing can influence host resistance to infection through its effect on cytokine production in addition to its role in cytotoxicity.

Indexed as

AnimalsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily B, Member 2beta 2-MicroglobulinCD8-Positive T-LymphocytesDendritic CellsGenetic Predisposition to DiseaseInterferon-gammaKiller Cells, NaturalMiceMice, KnockoutToxoplasmaToxoplasmosisATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily B, Member 2beta 2-MicroglobulinInterferon-gammaTap1 protein, mouse

Identifiers

PMID17923502
PMCPMC2118487
OpenAlexW2127416021

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.