Evidence map›Paper›PMID 21984699›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

The basis of distinctive IL-2- and IL-15-dependent signaling: weak CD122-dependent signaling favors CD8+ T central-memory cell survival but not T effector-memory cell development.

Iris Castro, Aixin Yu, Michael J Dee, Thomas R Malek

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. 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
2.1field-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, 65 citations in OpenAlex.

  1. T cell exhaustion in parasitic infections.Frontiers in immunology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. CD4Nature communications · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Regulatory T cells in the treatment of disease.Nature reviews. Drug discovery · 2018
    Review
  16. Article
  17. Review
  18. Article
  19. Immune network · 2018
    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

4 authors at 1 institution in 1 country.

Iris CastroDepartment of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, FL 33101, USA.
Aixin Yu
Michael J Dee
Thomas R Malek
University of Miami · US

Funding

REGULATION OF ANTI-TUMOR IMMUNITYP01CA109094 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DEYEV, VADIM V · 2007 to 2011
$6.2M
T cell immunity and cytokine receptor redundancyR01AI040114 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MALEK, THOMAS R · 1996 to 2005
$1.9M
T cell immunity and cytokine receptor signalingR56AI040114 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI MALEK, THOMAS R · 2008 to 2009
$765k
NCI NIH HHS CA109094NCI NIH HHS P01 CA109094NIAID NIH HHS AI040114NIAID NIH HHS R01 AI040114NIAID NIH HHS R56 AI040114
6 · The paper itself

Abstract

Recent work suggests that IL-2 and IL-15 induce distinctive levels of signaling through common receptor subunits and that such varied signaling directs the fate of Ag-activated CD8(+) T cells. In this study, we directly examined proximal signaling by IL-2 and IL-15 and CD8(+) T cell primary and memory responses as a consequence of varied CD122-dependent signaling. Initially, IL-2 and IL-15 induced similar p-STAT5 and p-S6 activation, but these activities were only sustained by IL-2. Transient IL-15-dependent signaling is due to limited expression of IL-15Rα. To investigate the outcome of varied CD122 signaling for CD8(+) T cell responses in vivo, OT-I T cells were used from mouse models where CD122 signals were attenuated by mutations within the cytoplasmic tail of CD122 or intrinsic survival function was provided in the absence of CD122 expression by transgenic Bcl-2. In the absence of CD122 signaling, generally normal primary response occurred, but the primed CD8(+) T cells were not maintained. In marked contrast, weak CD122 signaling supported development and survival of T central-memory (T(CM)) but not T effector-memory (T(EM)) cells. Transgenic expression of Bcl-2 in CD122(-/-) CD8(+) T cells also supported the survival and persistence of T(CM) cells but did not rescue T(EM) development. These data indicate that weak CD122 signals readily support T(CM) development largely through providing survival signals. However, stronger signals, independent of Bcl-2, are required for T(EM) development. Our findings are consistent with a model whereby low, intermediate, and high CD122 signaling support T(CM) memory survival, T(EM) programming, and terminal T effector cell differentiation, respectively.

Indexed as

Immunologic MemoryAnimalsCD8-Positive T-LymphocytesCells, CulturedCell SurvivalHumansInterleukin-15Interleukin-2Interleukin-2 Receptor beta SubunitMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicSignal TransductionT-Lymphocyte SubsetsIL2 protein, humanIl2rb protein, mouseInterleukin-15Interleukin-2Interleukin-2 Receptor beta Subunit

Identifiers

PMID21984699
PMCPMC3304468
OpenAlexW2099120617

What OpenQuestion holds

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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.