Evidence map›Paper›PMID 41057874›Full record

ArticleCell communication and signaling : CCS2025

Endothelial cell-derived apoptotic bodies modulate innate and adaptive immune responses during inflammation.

Caitlin L Vella, Pamali Fonseka, Emma J Grant, Stephanie F Rutter, Donia Y Abeid, Dilara C Ozkocak, Tien K Nguyen, Antony Vinh, Stephanie Paone, Grant R Drummond and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Apoptotic Bodies in Kidney Disease: Orchestrators of Inflammation, Fibrosis, and Repair.Journal of the American Society of Nephrology : JASN · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
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

16 authors.

Caitlin L VellaDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.ORCID http://orcid.org/0009-0009-6556-7861
Pamali FonsekaDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Emma J GrantDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Stephanie F RutterDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Donia Y AbeidDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Dilara C OzkocakDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Tien K NguyenDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Antony VinhResearch Centre for Extracellular Vesicles, La Trobe University, Bundoora, VIC, 3086, Australia.
Stephanie PaoneDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Grant R DrummondResearch Centre for Extracellular Vesicles, La Trobe University, Bundoora, VIC, 3086, Australia.
Christopher G SobeyResearch Centre for Extracellular Vesicles, La Trobe University, Bundoora, VIC, 3086, Australia.
Stephanie GrasDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Mark D HulettDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Suresh MathivananDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia.
Ivan K H PoonDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia. i.poon@latrobe.edu.au.
Amy A BaxterDepartment of Biochemistry and Chemistry, School of Agriculture, Biomedicine and Environment, La Trobe University, Bundoora, VIC, 3086, Australia. a.baxter@latrobe.edu.au.

Funding

Australian Research Council DE210101479National Health and Medical Research Council GNT1141732National Health and Medical Research Council GNT1159272National Health and Medical Research Council GNT1173662
6 · The paper itself

Abstract

Endothelial cells (ECs) act as gatekeepers and signalling hubs that coordinate communication between blood vessels and surrounding tissues by regulating vascular tone, immune responses and numerous other physiological processes. During vascular inflammation commonly associated with aging, atherosclerosis, diabetes and autoimmunity, a range of biological, environmental and physical stressors can induce activation and apoptosis of ECs. Apoptotic bodies (ApoBDs) are large (~ 1-5 μm), membrane‑bound extracellular vesicles generated solely through apoptotic cell disassembly, that are increasingly recognised as mediators of intercellular communication via the transfer of bioactive molecules to target cells. Although EC apoptosis is a central feature of vascular inflammatory disorders, the formation of EC‑derived ApoBDs and their immunomodulatory roles when formed in an inflammatory environment, remains poorly defined. This study aimed to characterise the functional properties of EC‑derived ApoBDs generated under inflammatory conditions in vitro. A proteomics analysis of EC‑derived ApoBDs revealed that EC‑ApoBDs generated during inflammation ('iApoBDs') were enriched in inflammatory cytokines/chemokines, adhesion molecules and antigen presentation machinery compared with non-inflammatory ('ApoBD') controls. Functionally, iApoBDs promoted monocyte chemotaxis via the release of MCP-1, while altered expression of the adhesion molecule ICAM-1 enhanced efferocytosis by macrophages in vitro and in vivo. Furthermore, iApoBDs generated from antigen-pulsed HUVECs promoted IFN‑𝛾 expression by peptide specific CD8 T cells in an in vitro model of antigen presentation. These findings demonstrate that within an inflammatory setting, apoptotic ECs can participate in continued communication with their environment via the generation of ApoBDs, thereby modulating innate and adaptive immune processes. The formation of ApoBDs by ECs may serve as a target for therapeutic interventions in inflammatory vascular diseases.

Indexed as

Adaptive ImmunityApoptosisEndothelial CellsExtracellular VesiclesImmunity, InnateInflammationHumansHuman Umbilical Vein Endothelial CellsApoptosisApoptotic bodiesEfferocytosisEndothelial cellsExtracellular vesiclesInflammation

Identifiers

PMID41057874
PMCPMC12502297

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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.