Immune interplay between sepsis and haematological malignancies.

Stéphanie Pons, Morgane Grosset, Emmanuelle Touze, Lara Zafrani

Abstract readReview

In one paragraph

Review in Intensive care medicine experimental, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

1 citing paper in PubMed.

Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026
Review

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.

Stéphanie PonsUMR 1342, INSERM, Institut de recherche Saint-Louis, Université Paris Cité, Paris, France.

Morgane GrossetUMR 1342, INSERM, Institut de recherche Saint-Louis, Université Paris Cité, Paris, France.

Emmanuelle TouzeUMR 1342, INSERM, Institut de recherche Saint-Louis, Université Paris Cité, Paris, France.

Lara ZafraniUMR 1342, INSERM, Institut de recherche Saint-Louis, Université Paris Cité, Paris, France. lara.zafrani@aphp.fr.ORCID http://orcid.org/0000-0002-7805-3116

Funding

Agence Nationale de la Recherche - Program "Emergence" ANR-18-IdEx-0001Fondation de l'Avenir pour la Recherche Médicale Appliquée AP-RM-23-007

6 · The paper itself

Abstract

Haematological malignancies (HMs) are characterized by profound immune dysregulation, which increases susceptibility to sepsis. This dysregulation arises from the underlying disease and may be exacerbated by treatments. Sepsis itself induces a biphasic immune response, with an initial hyperinflammatory phase followed by prolonged immunosuppression that can persist for months or years, potentially impacting the course of HMs. This review examines the reciprocal interactions between HMs and sepsis, focusing on innate and adaptive immune alterations, the influence of malignancy-associated dysbiosis, and insights gained from experimental models. In addition, we discuss how sepsis-induced systemic inflammation may influence the progression of the underlying malignancy, through pro-inflammatory cytokine signaling and alterations in the bone marrow microenvironment. Understanding these complex interactions may provide a framework for mitigating infection-related complications and for exploring their influence on the natural history and progression of HM.

Indexed as

Acute myeloid leukemiaHaematological malignanciesImmunosuppressionKeywordsSepsis

Identifiers

PMID42047954

DOI10.1186/s40635-026-00904-6

PMCPMC13125539

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.