Evidence map›Paper›PMID 25940792›Full record

ArticleBritish journal of haematology2015

Chronic lymphocytic leukaemia induces an exhausted T cell phenotype in the TCL1 transgenic mouse model.

Franz J Gassner, Nadja Zaborsky, Kemal Catakovic, Stefan Rebhandl, Michael Huemer, Alexander Egle, Tanja N Hartmann, Richard Greil, Roland Geisberger

Open access · hybridAbstract read
In one paragraph

Article in British journal of haematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Expanded antigen-experienced CD160Journal for immunotherapy of cancer · 2021
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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

9 authors at 1 institution in 1 country.

Franz J GassnerLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Nadja ZaborskyLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Kemal CatakovicLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Stefan RebhandlLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Michael HuemerLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Alexander EgleLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Tanja N HartmannLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Richard GreilLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Roland GeisbergerLaboratory for Immunological and Molecular Cancer Research, 3rd Medical Department with Haematology, Medical Oncology, Haemostaseology, Infectiology and Rheumatology, Oncologic Centre, Paracelsus Medical University, Salzburg, Austria.
Paracelsus Medical University · AT

Funding

Austrian Science Fund FWF I 1299
6 · The paper itself

Abstract

Although chronic lymphocytic leukaemia (CLL) is a B cell malignancy, earlier studies have indicated a role of T cells in tumour growth and disease progression. In particular, the functional silencing of antigen-experienced T cells, called T cell exhaustion, has become implicated in immune evasion in CLL. In this study, we tested whether T cell exhaustion is recapitulated in the TCL1(tg) mouse model for CLL. We show that T cells express high levels of the inhibitory exhaustion markers programmed cell death 1 (PDCD1, also termed PD-1) and lymphocyte-activation gene 3 (LAG3), whereas CLL cells express high levels of CD274 (also termed PD-ligand 1). In addition, the fraction of exhausted T cells increases with CLL progression. Finally, we demonstrate that exhausted T cells are reinvigorated towards CLL cytotoxicity by inhibition of PDCD1/CD274 interaction in vivo. These results suggest that T cell exhaustion contributes to CLL pathogenesis and that interference with PDCD1/CD274 signalling holds high potential for therapeutic approaches.

Indexed as

AnimalsGene Expression Regulation, LeukemicLeukemia, Lymphocytic, Chronic, B-CellMiceMice, TransgenicNeoplasm ProteinsNeoplasms, ExperimentalSignal TransductionT-LymphocytesNeoplasm Proteinschemoimmunotherapychronic lymphocytic leukaemiaPDCD1T cell exhaustiontumour surveillance

Identifiers

PMID25940792
PMCPMC4687418
OpenAlexW1940329735

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.