Evidence map›Paper›PMID 16614074›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Lack of IL-15 results in the suboptimal priming of CD4+ T cell response against an intracellular parasite.

Crescent L Combe, Magali M Moretto, Joseph D Schwartzman, Jason P Gigley, David J Bzik, Imtiaz A Khan

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Advances towards the completeFaculty reviews · 2023
    Review
  2. Review
  3. Influence of the Host and Parasite Strain on the Immune Response DuringFrontiers in cellular and infection microbiology · 2020
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. CD8 T Cells and Toxoplasma gondii: A New Paradigm.Journal of parasitology research · 2011
    Article
  16. Article
  17. Article
  18. Review
  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

6 authors at 1 institution in 1 country.

Crescent L CombeDepartment of Microbiology, Parasitology, and Immunology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Magali M Moretto
Joseph D Schwartzman
Jason P Gigley
David J Bzik
Imtiaz A Khan
Louisiana State University Health Sciences Center New Orleans · US

Funding

LONG TERM IMMUNITY AGAINST TOXOPLASMOSISR01AI033325 · NIAID · LOUISIANA STATE UNIV HSC NEW ORLEANS · PI KHAN, IMTIAZ AHMED · 1998 to 2020
$6.2M
T GONDII--PYRIMIDINE SYNTHESIS AS A CHEMOTHERAPY TARGETR01AI041930 · NIAID · DARTMOUTH COLLEGE · PI BZIK, DAVID J · 1997 to 2013
$4.2M
Attenuated T.gondii as a Vector for HIV VaccinesR21AI052026 · NIAID · DARTMOUTH COLLEGE · PI BZIK, DAVID J · 2002 to 2003
$395k
LONG TERM IMMUNITY AGAINST TOXOPLASMOSISR21AI033325 · NIAID · DARTMOUTH COLLEGE · PI KHAN, IMTIAZ AHMED · 1997 to 1997
–
TOXOPLASMA GONDII MEDIATED IMMUNOSUPPRESSIONR29AI033325 · NIAID · DARTMOUTH COLLEGE · PI KHAN, IMTIAZ AHMED · 1992 to 1996
–
NIAID NIH HHS AI33325NIAID NIH HHS AI41930NIAID NIH HHS R01 AI033325NIAID NIH HHS R01 AI041930NIAID NIH HHS R21 AI052026
6 · The paper itself

Abstract

IFN-gamma-producing CD4+ T cells, although important for protection against acute Toxoplasma gondii infection, can cause gut pathology, which may prove to be detrimental for host survival. Here we show that mice lacking IL-15 gene develop a down-regulated IFN-gamma-producing CD4+ T cell response against the parasite, which leads to a reduction in gut necrosis and increased level of survival against infection. Moreover, transfer of immune CD4+ T cells from WT to IL-15-/- mice reversed inhibition of gut pathology and caused mortality equivalent to levels of parental WT mice. Down-regulated CD4+ T cell response in the absence of IL-15, manifested as reduced antigen-specific proliferation, was due to defective priming of the T cell subset by dendritic cells (DCs) of these animals. When stimulated with antigen-pulsed DCs from WT mice, CD4+ T cells from IL-15-/- mice were primed optimally, and robust proliferation of these cells was observed. A defect in the DCs of knockout mice was further confirmed by their reduced ability to produce IL-12 upon stimulation with Toxoplasma lysate antigen. Addition of exogenous IL-15 to DC cultures from knockout mice led to increased IL-12 production by these cells and restored their ability to prime an optimal parasite-specific CD4+ T cell response. To our knowledge, this is the first demonstration of the role of IL-15 in the development of CD4+ T cell immunity against an intracellular pathogen. Furthermore, based on these observations, targeting of IL-15 should have a beneficial effect on individuals suffering from CD4+ T cell-mediated autoimmune diseases.

Indexed as

Adoptive TransferAnimalsCD4-Positive T-LymphocytesDendritic CellsFemaleHumansInterferon-gammaInterleukin-12Interleukin-15MiceMice, Inbred C57BLMice, KnockoutToxoplasmaToxoplasmosis, AnimalInterferon-gammaInterleukin-12Interleukin-15

Identifiers

PMID16614074
PMCPMC1458934
OpenAlexW1971513700

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.