Evidence map›Paper›PMID 19605694›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

The magnitude of CD4+ T cell recall responses is controlled by the duration of the secondary stimulus.

Eugene V Ravkov, Matthew A Williams

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019
    Article
  7. Article
  8. Article
  9. Experimental Hyalohyphomycosis byFrontiers in microbiology · 2017
    Article
  10. Article
  11. The Timing of T Cell Priming and Cycling.Frontiers in immunology · 2015
    Review
  12. Article
  13. Article
  14. CD4 T-cell memory generation and maintenance.Critical reviews in immunology · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 2 countries.

Eugene V RavkovDepartment of Pathology, University of Utah, Salt Lake City, UT 84112, USA.
Matthew A Williams
University of Utah · US

Funding

The role of antigenic stimulatory strength in the selection and differentiation oR01AI080830 · NIAID · UNIVERSITY OF UTAH · PI WILLIAMS, MATTHEW A · 2010 to 2014
$1.8M
The role of IL-2 in promoting CD8 memory T cell responsivenessK22AI071112 · NIAID · UNIVERSITY OF UTAH · PI WILLIAMS, MATTHEW A · 2007 to 2008
$268k
NIAID NIH HHS K22 AI071112NIAID NIH HHS K22AI071112NIAID NIH HHS R01 AI080830
6 · The paper itself

Abstract

The parameters controlling the generation of robust CD4(+) T cell recall responses remain poorly defined. In this study, we compare recall responses by CD4(+) and CD8(+) memory T cells following rechallenge. Homologous rechallenge of mice immune to either lymphocytic choriomeningitis virus or Listeria monocytogenes results in robust CD8(+) T cell recall responses but poor boosting of CD4(+) T cell recall responses in the same host. In contrast, heterologous rechallenge with a pathogen sharing only a CD4(+) T cell epitope results in robust boosting of CD4(+) T cell recall responses. The disparity in CD4(+) and CD8(+) T cell recall responses cannot be attributed to competition for growth factors or APCs, as robust CD4(+) and CD8(+) T cell recall responses can be simultaneously induced following rechallenge with peptide-pulsed dendritic cells. Instead, CD4(+) T cell recall responses are dependent on the duration of the secondary challenge. Increasing the rechallenge dose results in more potent boosting of CD4(+) T cell recall responses and artificially limiting the duration of secondary infection following heterologous rechallenge adversely impacts the magnitude of CD4(+) T cell, but not CD8(+) T cell, recall responses. These findings suggest that rapid pathogen clearance by secondary CTL following homologous rechallenge prevents optimal boosting of CD4(+) T cell responses and therefore have important practical implications in the design of vaccination and boosting strategies aimed at promoting CD4(+) T cell-mediated protection.

Indexed as

Immunization, SecondaryImmunologic MemoryAmino Acid SequenceAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell LineCell ProliferationCricetinaeListeria monocytogenesLymphocyte ActivationLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, TransgenicMolecular Sequence DataOvalbumin

Identifiers

PMID19605694
PMCPMC2819348
OpenAlexW2103678990

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.