Evidence map›Paper›PMID 29225343›Full record

ReviewNature reviews. Nephrology2018

Advances in the understanding and treatment of sepsis-induced immunosuppression.

Fabienne Venet, Guillaume Monneret

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 608 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
608citing papers in PubMed, 5 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

608 citing papers in PubMed, 5 syntheses or guidelines pooled it.

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  13. Clinical and laboratory predictors of mortality in Fournier's gangrene: prognostic role of the HALP score.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2026
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548 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Fabienne VenetHospices Civils de Lyon, Hôpital Edouard Herriot, Immunology Department, Flow Division, 69003 Lyon, France.
Guillaume MonneretHospices Civils de Lyon, Hôpital Edouard Herriot, Immunology Department, Flow Division, 69003 Lyon, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is defined as a life-threatening organ dysfunction that is caused by a dysregulated host response to infection. Sepsis can induce acute kidney injury and multiple organ failures and represents the most common cause of death in the intensive care unit. Sepsis initiates a complex immune response that varies over time, with the concomitant occurrence of both pro-inflammatory and anti-inflammatory mechanisms. As a result, most patients with sepsis rapidly display signs of profound immunosuppression, which is associated with deleterious consequences. Scientific advances have highlighted the role of metabolic failure, epigenetic reprogramming, myeloid-derived suppressor cells, immature suppressive neutrophils and immune alterations in primary lymphoid organs (the thymus and bone marrow) in sepsis. An improved understanding of the mechanisms underlying this immunosuppression as well as of the similarities between sepsis-induced immunosuppression and immune defects in cancer or immunosenescence has led to novel therapeutic strategies aimed at stimulating immune function in patients with sepsis. Trials assessing the therapeutic benefit of IL-7, granulocyte-macrophage colony-stimulating factor (GM-CSF) and antibodies against programmed cell death protein 1 (PD1) and programmed cell death 1 ligand 1 (PDL1) for the treatment of sepsis are in progress. The reappraisal of sepsis pathophysiology has also resulted in a novel approach to the design of clinical trials evaluating sepsis treatments, based on an evaluation of the immune status and biomarker-based stratification of patients.

Indexed as

Adjuvants, ImmunologicAnti-Inflammatory AgentsApoptosisAutophagyBiomarkersB-LymphocytesDendritic CellsEpigenesis, GeneticGranulocyte-Macrophage Colony-Stimulating FactorHumansImmune ToleranceImmunosenescenceInterferon-gammaInterleukin-17LeukocytesMonocytesAdjuvants, ImmunologicAnti-Inflammatory AgentsBiomarkersGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaInterleukin-17

Identifiers

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.