Evidence map›Paper›PMID 30037849›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2018

Cigarette Smoke-Induced Emphysema Exhausts Early Cytotoxic CD8

Dimitra Kerdidani, Sophia Magkouta, Panagiotis Chouvardas, Vassiliki Karavana, Konstantinos Glynos, Fani Roumelioti, Spyros Zakynthinos, Els Wauters, Wim Janssens, Diether Lambrechts and 2 more

Abstract read
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In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  5. Antiviral CD8The European respiratory journal · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 3 countries.

Dimitra KerdidaniDivision of Immunology, Biomedical Sciences Research Center 'Alexander Fleming,' 16672 Vari, Athens, Greece.
Sophia MagkoutaDepartment of Intensive Care Medicine, School of Medicine, National and Kapodistrian University of Athens, 10679 Athens, Greece.
Panagiotis ChouvardasDivision of Immunology, Biomedical Sciences Research Center 'Alexander Fleming,' 16672 Vari, Athens, Greece.
Vassiliki KaravanaDepartment of Intensive Care Medicine, School of Medicine, National and Kapodistrian University of Athens, 10679 Athens, Greece.ORCID 0000-0002-6628-4419
Konstantinos GlynosDepartment of Intensive Care Medicine, School of Medicine, National and Kapodistrian University of Athens, 10679 Athens, Greece.
Fani RoumeliotiDivision of Immunology, Biomedical Sciences Research Center 'Alexander Fleming,' 16672 Vari, Athens, Greece.
Spyros ZakynthinosDepartment of Intensive Care Medicine, School of Medicine, National and Kapodistrian University of Athens, 10679 Athens, Greece.
Els WautersRespiratory Oncology Unit, University Hospitals KU Leuven, 3000 Leuven, Belgium.
Wim JanssensRespiratory Oncology Unit, University Hospitals KU Leuven, 3000 Leuven, Belgium.
Diether LambrechtsVIB Center for Cancer Biology, VIB, 3000 Leuven, Belgium; and.
George KolliasDivision of Immunology, Biomedical Sciences Research Center 'Alexander Fleming,' 16672 Vari, Athens, Greece.
Maria TsoumakidouDivision of Immunology, Biomedical Sciences Research Center 'Alexander Fleming,' 16672 Vari, Athens, Greece; tsoumakidou@fleming.gr.ORCID 0000-0001-7959-4793
National and Kapodistrian University of Athens · GRVIB-KU Leuven Center for Cancer Biology · BEAlexander Fleming Biomedical Sciences Research Center · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease is a chronic inflammatory disorder with an increased incidence of lung cancer. The emphysema component of chronic obstructive pulmonary disease confers the greatest proportion to lung cancer risk. Although tumors create inflammatory conditions to escape immunity, the immunological responses that control growth of nascent cancer cells in pre-established inflammatory microenvironments are unknown. In this study, we addressed this issue by implanting OVA-expressing cancer cells in the lungs of mice with cigarette smoke-induced emphysema. Emphysema augmented the growth of cancer cells, an effect that was dependent on T cytotoxic cells. OVA-specific OTI T cells showed early signs of exhaustion upon transfer in emphysema tumor hosts that was largely irreversible because sorting, expansion, and adoptive transfer failed to restore their antitumor activity. Increased numbers of PD-L1- and IDO-positive CD11c

Indexed as

Adoptive TransferAnimalsCD8-Positive T-LymphocytesCigarette SmokingLung NeoplasmsMiceMice, TransgenicPulmonary Emphysema

Identifiers

PMID30037849
OpenAlexW2884238668

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.