Evidence map›Paper›PMID 25257362›Full record

ArticleNature reviews. Immunology2014

T cell differentiation in chronic infection and cancer: functional adaptation or exhaustion?

Daniel E Speiser, Daniel T Utzschneider, Susanne G Oberle, Christian Münz, Pedro Romero, Dietmar Zehn

Abstract read
PubMed Publisher
In one paragraph

Article in Nature reviews. Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 1 pooled it
–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

190 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. PD-1Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Trial
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. T cell adaptation in chronic infections and tumors.Cellular & molecular immunology · 2026
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

130 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

6 authors.

Daniel E SpeiserLudwig Cancer Research Center, Department of Oncology, University of Lausanne, 1011 Lausanne, Switzerland.
Daniel T UtzschneiderSwiss Vaccine Research Institute, Centre des laboratoires d'Epalinges, 1066 Epalinges, Switzerland, and the Division of Immunology and Allergy, Department of Medicine, Lausanne University Hospital, 1011 Lausanne, Switzerland.
Susanne G OberleSwiss Vaccine Research Institute, Centre des laboratoires d'Epalinges, 1066 Epalinges, Switzerland, and the Division of Immunology and Allergy, Department of Medicine, Lausanne University Hospital, 1011 Lausanne, Switzerland.
Christian MünzInstitute for Experimental Immunology, University of Zürich, CH-8057 Zürich, Switzerland.
Pedro RomeroLudwig Cancer Research Center, Department of Oncology, University of Lausanne, 1011 Lausanne, Switzerland.
Dietmar ZehnSwiss Vaccine Research Institute, Centre des laboratoires d'Epalinges, 1066 Epalinges, Switzerland, and the Division of Immunology and Allergy, Department of Medicine, Lausanne University Hospital, 1011 Lausanne, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic viral infections and malignant tumours induce T cells that have a reduced ability to secrete effector cytokines and have upregulated expression of the inhibitory receptor PD1 (programmed cell death protein 1). These features have so far been considered to mark terminally differentiated 'exhausted' T cells. However, several recent clinical and experimental observations indicate that phenotypically exhausted T cells can still mediate a crucial level of pathogen or tumour control. In this Opinion article, we propose that the exhausted phenotype results from a differentiation process in which T cells stably adjust their effector capacity to the needs of chronic infection. We argue that this phenotype is optimized to cause minimal tissue damage while still mediating a critical level of pathogen control. In contrast to the presently held view of functional exhaustion, this new concept better reflects the pathophysiology and clinical manifestations of persisting infections, and it provides a rationale for emerging therapies that enhance T cell activity in chronic infection and cancer by blocking inhibitory receptors.

Indexed as

CD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell DifferentiationChronic DiseaseCytokinesHumansImmunologic MemoryLymphocyte ActivationNeoplasmsProgrammed Cell Death 1 ReceptorVirus DiseasesCytokinesPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID25257362

What OpenQuestion holds

Textmetadata
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.