Evidence map›Paper›PMID 20208003›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Persistent gamma-herpesvirus infection induces a CD4 T cell response containing functionally distinct effector populations.

Kathleen A Stuller, Stephanie S Cush, Emilio Flaño

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cytotoxic CD4Frontiers in immunology · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Cytotoxic CD4 T cells in antiviral immunity.Journal of biomedicine & biotechnology · 2011
    Review
  20. Cytolytic CD4(+) T cells in viral immunity.Expert review of vaccines · 2010
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kathleen A StullerCenter for Vaccines and Immunity, The Research Institute at Nationwide Children's Hospital, Columbus, OH 43205, USA.
Stephanie S Cush
Emilio Flaño
Nationwide Children's Hospital · US

Funding

Gamma-herpesvirus infection of dendritic cellsR01AI059603 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI FLANO, EMILIO · 2005 to 2009
$1.4M
Dendritic Cell Function in Lung Viral InfectionR56AI059603 · NIAID · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI FLANO, EMILIO · 2011 to 2011
$326k
NIAID NIH HHS AI-59603NIAID NIH HHS R01 AI059603NIAID NIH HHS R56 AI059603
6 · The paper itself

Abstract

The direct effector mechanisms of CD4 T cells during gamma-herpesvirus 68 (gammaHV68)-persistent infection are less well understood than those of their CD8 T cell counterparts, although there is substantial evidence that CD4 T cells are critical for the control of persistent gamma-herpesvirus infection. Our results show that in gammaHV68-persistently infected mice, CD4 T cells are not cytokine polyfunctional, but there is a division of labor in the CD4 T cell compartment in which CD4 T cells polarize toward two distinct populations with different effector functions: IFN-gamma producers and CD107(+) cytolytic effectors. These two CD4 T cell effector populations degranulate and produce IFN-gamma during steady state without need for exogenous antigenic restimulation, which is fundamentally different from that observed with gammaHV68-specific CD8 T cells. By using anti-IFN-gamma Ab depletions and IFN-gamma-deficient mice, we show that CD4 T cell-mediated cytotoxicity in vivo is not dependent on IFN-gamma activity. In addition, our data show that purified CD4 T cells isolated from gammaHV68-latently infected mice have the capacity to inhibit gammaHV68 reactivation from latency. Our results support the concept that CD4 T cells are critical effectors for the control of gamma-herpesvirus latent infection, and they mediate this effect by two independent mechanisms: IFN-gamma production and cytotoxicity.

Indexed as

AnimalsCD4-Positive T-LymphocytesCell SeparationCytotoxicity, ImmunologicEnzyme-Linked Immunosorbent AssayFlow CytometryHerpesviridae InfectionsInterferon-gammaMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutRhadinovirusT-Lymphocyte SubsetsVirus LatencyInterferon-gamma

Identifiers

PMID20208003
PMCPMC3044337
OpenAlexW1784947136

What OpenQuestion holds

Textmetadata
LicenceTDM
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.