Evidence map›Paper›PMID 26163589›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Persistent Antigen and Prolonged AKT-mTORC1 Activation Underlie Memory CD8 T Cell Impairment in the Absence of CD4 T Cells.

Yingzhong Li, Chase Shen, Bingdong Zhu, Feng Shi, Herman N Eisen, Jianzhu Chen

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Helpless Priming Sends CD8Frontiers in immunology · 2020
    Article
  7. Review
  8. iCaFrontiers in immunology · 2020
    Article
  9. Article
  10. Article
  11. Review
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.

Yingzhong LiDepartment of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Chase ShenDepartment of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Bingdong ZhuDepartment of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Feng ShiDepartment of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Herman N EisenDepartment of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139.
Jianzhu ChenDepartment of Biology, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139 jchen@mit.edu.

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Development and Maintenance of Memory CD8 T CellsR01AI069208 · NIAID · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI CHEN, JIANZHU · 2006 to 2010
$2.0M
NCI NIH HHS P30 CA014051NCI NIH HHS P30-CA14051NIAID NIH HHS AI69208NIAID NIH HHS R01 AI069208
6 · The paper itself

Abstract

Recall responses by memory CD8 T cells are impaired in the absence of CD4 T cells. Although several mechanisms have been proposed, the molecular basis is still largely unknown. Using a local influenza virus infection in the respiratory tract and the lung of CD4(-/-) mice, we show that memory CD8 T cell impairment is limited to the lungs and the lung-draining lymph nodes, where viral Ags are unusually persistent and abundant in these mice. Persistent Ag exposure results in prolonged activation of the AKT-mTORC1 pathway in Ag-specific CD8 T cells, favoring their development into effector memory T cells at the expense of central memory T cells, and inhibition of mTORC1 by rapamycin largely corrects the impairment by promoting central memory T cell development. The findings suggest that the prolonged AKT-mTORC1 activation driven by persistent Ag is a critical mechanism underlying the impaired memory CD8 T cell development and responses in the absence of CD4 T cells.

Indexed as

Immunologic MemoryAnimalsAntigensCD4 AntigensCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesImmunophenotypingLymphocyte ActivationMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMice, TransgenicMultiprotein ComplexesOrthomyxoviridaeOrthomyxoviridae InfectionsPhenotypeAntigensCD4 AntigensMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProto-Oncogene Proteins c-aktSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID26163589
PMCPMC4530017

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.