Evidence map›Paper›PMID 24739177›Full record

ArticleBiophysical journal2014

A general functional response of cytotoxic T lymphocyte-mediated killing of target cells.

Saikrishna Gadhamsetty, Athanasius F M Marée, Joost B Beltman, Rob J de Boer

Abstract read
In one paragraph

Article in Biophysical journal, 2014. 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
–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

29 citing papers in PubMed.

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  13. Towards multiscale modeling of the CD8Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
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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

4 authors.

Saikrishna GadhamsettyTheoretical Biology and Bioinformatics, Utrecht University, Utrecht, the Netherlands. Electronic address: s.gadhamsetty@uu.nl.
Athanasius F M MaréeDepartment of Computational and Systems Biology, John Innes Centre, Norwich, United Kingdom.
Joost B BeltmanTheoretical Biology and Bioinformatics, Utrecht University, Utrecht, the Netherlands; Division of Immunology, the Netherlands Cancer Institute, Amsterdam, the Netherlands.
Rob J de BoerTheoretical Biology and Bioinformatics, Utrecht University, Utrecht, the Netherlands.

Funding

Biotechnology and Biological Sciences Research Council BBS/E/J/000C0645
6 · The paper itself

Abstract

Cytotoxic T lymphocytes (CTLs) kill virus-infected cells and tumor cells, and play a critical role in immune protection. Our knowledge of how the CTL killing efficiency varies with CTL and target cell numbers is limited. Here, we simulate a region of lymphoid tissue using a cellular Potts model to characterize the functional response of CTL killing of target cells, and find that the total killing rate saturates both with the CTL and the target cell densities. The relative saturation in CTL and target cell densities is determined by whether a CTL can kill multiple target cells at the same time, and whether a target cell can be killed by many CTLs together. We find that all the studied regimes can be well described by a double-saturation (DS) function with two different saturation constants. We show that this DS model can be mechanistically derived for the cases where target cells are killed by a single CTL. For the other cases, a biological interpretation of the parameters is still possible. Our results imply that this DS function can be used as a tool to predict the cellular interactions in cytotoxicity data.

Indexed as

Cytotoxicity, ImmunologicComputer SimulationConfidence IntervalsHumansImmunological SynapsesLymphocyte CountModels, ImmunologicalSurface TensionT-Lymphocytes, Cytotoxic

Identifiers

PMID24739177
PMCPMC4008826

What OpenQuestion holds

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Registered trials

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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.