Evidence map›Paper›PMID 30730978›Full record

ArticlePloS one2019

Sepsis induces long-lasting impairments in CD4+ T-cell responses despite rapid numerical recovery of T-lymphocyte populations.

Christoph Ammer-Herrmenau, Upasana Kulkarni, Nico Andreas, Martin Ungelenk, Sarina Ravens, Christian Hübner, Angela Kather, Ingo Kurth, Michael Bauer, Thomas Kamradt

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

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  12. Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024
    Review
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  14. Observational
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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

10 authors at 2 institutions in 1 country.

Christoph Ammer-HerrmenauInstitute of Immunology, Jena University Hospital, Jena, Germany, United States of America.
Upasana KulkarniInstitute of Immunology, Jena University Hospital, Jena, Germany, United States of America.
Nico AndreasInstitute of Immunology, Jena University Hospital, Jena, Germany, United States of America.ORCID 0000-0002-4591-7037
Martin UngelenkInstitute of Human Genetics, Jena University Hospital, Jena, Germany.
Sarina RavensInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Christian HübnerInstitute of Human Genetics, Jena University Hospital, Jena, Germany.
Angela KatherInstitute of Immunology, Jena University Hospital, Jena, Germany, United States of America.
Ingo KurthInstitute of Human Genetics, Jena University Hospital, Jena, Germany.
Michael BauerDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Thomas KamradtInstitute of Immunology, Jena University Hospital, Jena, Germany, United States of America.ORCID 0000-0001-8443-5893
Jena University Hospital · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Massive apoptosis of lymphocytes is a hallmark of sepsis. The resulting immunosuppression is associated with secondary infections, which are often lethal. Moreover, sepsis-survivors are burdened with increased morbidity and mortality for several years after the sepsis episode. The duration and clinical consequences of sepsis induced-immunosuppression are currently unknown. We have used the mouse model of peritoneal contamination and infection (PCI) to investigate the quantitative and qualitative recovery of T lymphocytes for 3.5 months after sepsis with or without IL-7 treatment. Thymic output and the numbers of naive and effector/memory CD4+ and CD8+ lymphocytes quickly recovered after sepsis. IL-7 treatment resulted in an accelerated recovery of CD8+ lymphocytes. Next generation sequencing revealed no significant narrowing of the T cell receptor repertoire 3.5 months after sepsis. In contrast, detailed functional analyses of T helper (Th)-cell responses towards a fungal antigen revealed a significant loss of Th cells. Whereas cytokine production was not impaired at the single cell level, the absolute number of Th cells specific for the fungal antigen was reduced. Our data indicate a clinically relevant loss of pathogen-specific T cell clones after sepsis. Given the small number of naive T lymphocytes specific for a given antigen, this decrement of T cell clones remains undetected even by sensitive methods such as deep sequencing. Taken together, our data are compatible with long lasting impairments in CD4+ T-cell responses after sepsis despite rapid recovery of T lymphocyte populations.

Indexed as

AnimalsAntigens, FungalCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCells, CulturedDisease Models, AnimalHumansImmunologic MemoryInterleukin-7Lymphocyte CountMiceMice, Inbred C57BLReceptors, Antigen, T-CellSepsisAntigens, FungalInterleukin-7Receptors, Antigen, T-Cell

Identifiers

PMID30730978
PMCPMC6366777
OpenAlexW2911583817

What OpenQuestion holds

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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.