Evidence map›Paper›PMID 21187318›Full record

ArticleThe Journal of experimental medicine2011

Antiviral CD8+ T cell effector activities in situ are regulated by target cell type.

Matthew M Hufford, Taeg S Kim, Jie Sun, Thomas J Braciale

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

85 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Triphasic production of IFNDiscovery immunology · 2023
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Immune system response during viral Infections: Immunomodulators, cytokine storm (CS) and Immunotherapeutics in COVID-19.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
    Review
  12. Tissue-resident CD4Science immunology · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. PD-1Science immunology · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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.

Matthew M HuffordBeirne B. Carter Center for Immunology Research, Department of Microbiology, University of Virginia, Charlottesville, VA 22904, USA.
Taeg S Kim
Jie Sun
Thomas J Braciale
Carter Center · US

Funding

INTERDISCIPLINARY TRAINING PROGRAM IN IMMUNOLOGYT32AI007496 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Michael G. Brown, Coleen A McNamara · 1995 to 2026
$10.2M
Regulation of CD8+ T cell responses via liver NK-DC crosstalkU19AI083024 · NIAID · UNIVERSITY OF VIRGINIA · PI LANNIGAN, JOANNE A · 2009 to 2013
$8.1M
CYTOTOXIC T LYMPHOCYTE RESPONSE TO INFLUENZA VIRUSR01AI015608 · NIAID · WASHINGTON UNIVERSITY · PI BRACIALE, THOMAS J · 1985 to 2017
$5.7M
T Cell Function in Pulmonary Viral Pulmonary Infection and InjuryR01HL033391 · NHLBI · WASHINGTON UNIVERSITY · PI BRACIALE, THOMAS J · 1985 to 2012
$4.3M
Global Biothreats Training ProgramT32AI055432 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI CRISS, ALISON K, PETRI, WILLIAM A · 2003 to 2022
$4.0M
IMMUNOBIOLOGY OF EXPERIMENTAL RSV INFECTIONR01AI037293 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI BRACIALE, THOMAS J · 1994 to 2007
$2.3M
NHLBI NIH HHS R01 HL033391NHLBI NIH HHS R01 HL-33391NIAID NIH HHS R01 AI015608NIAID NIH HHS R01 AI037293NIAID NIH HHS R01 AI-15608NIAID NIH HHS R01 AI-37293NIAID NIH HHS T32 AI007496NIAID NIH HHS T32 AI007496-13NIAID NIH HHS T32 AI055432NIAID NIH HHS U19 AI083024NIAID NIH HHS U-19 AI-83024
6 · The paper itself

Abstract

Cytotoxic T lymphocytes (CTLs) play a prominent role in the resolution of viral infections through their capacity both to mediate contact-dependent lysis of infected cells and to release soluble proinflammatory cytokines and chemokines. The factors controlling these antiviral effector activities in vivo at infection sites are ill defined. Using a mouse model of influenza infection, we observed that the expression of CTL effector activity in the infected lungs is dictated by the target cell type encountered. CD45(+) lung infiltrating inflammatory mononuclear cells, particularly CD11c(hi) dendritic cells, trigger both CTL cytotoxicity and release of inflammatory mediators, whereas CD45(-) influenza-infected respiratory epithelial cells stimulate only CTL cytotoxicity. CTL proinflammatory mediator release is modulated by co-stimulatory ligands (CD80 and CD86) expressed by the CD45(+) inflammatory cells. These findings suggest novel mechanisms of control of CTL effector activity and have potentially important implications for the control of excess pulmonary inflammation and immunopathology while preserving optimal viral clearance during respiratory virus infections.

Indexed as

AnimalsCD11 AntigensCD8-Positive T-LymphocytesCoculture TechniquesFemaleHistocompatibility Antigens Class IInfluenza A virusInterferon-gammaKineticsLeukocyte Common AntigensMiceCD11 AntigensHistocompatibility Antigens Class IInterferon-gammaLeukocyte Common AntigensPtprc protein, mouse

Identifiers

PMID21187318
PMCPMC3023137
OpenAlexW2162203679

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.