Evidence map›Paper›PMID 39885580›Full record

ArticleJournal of nanobiotechnology2025

Extracellular vesicle surface engineering with integrins (ITGAL & ITGB2) to specifically target ICAM-1-expressing endothelial cells.

Markus Bergqvist, Kyong-Su Park, Nasibeh Karimi, Lijuan Yu, Cecilia Lässer, Jan Lötvall

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Does extracellular vesicle specificity truly exist?Cell communication and signaling : CCS · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. 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

6 authors.

Markus BergqvistKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0009-0003-5716-3716
Kyong-Su ParkKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-0902-7800
Nasibeh KarimiKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-1499-6876
Lijuan YuKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-3558-3800
Cecilia LässerKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0003-1279-1746
Jan LötvallKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. jan.lotvall@gu.se.ORCID http://orcid.org/0000-0001-9195-9249

Funding

Hjärt-Lungfonden 244018078Vetenskapsrådet 254018063
6 · The paper itself

Abstract

Extracellular vesicles (EVs) are taken up by most cells, however specific or preferential cell targeting remains a hurdle. This study aims to develop an EV that targets cells involved in inflammation, specifically those expressing intercellular adhesion molecule-1 (ICAM-1). To target these cells, we overexpress the ICAM-1 binding receptor "lymphocyte function-associated antigen-1" (LFA-1) in HEK293F cells, by sequential transfection of plasmids of the two LFA-1 subunits, ITGAL and ITGB2 (CD11a and CD18). The LFA-1 receptor was strongly overexpressed on the EVs released by the transfected cells. We further loaded these EVs with a therapeutic peptide, targeting myeloid differentiation primary response 88 (Myd88; EV

Indexed as

CD11a AntigenCD18 AntigensEndothelial CellsExtracellular VesiclesIntercellular Adhesion Molecule-1HEK293 CellsHumansHuman Umbilical Vein Endothelial CellsInterleukin-8Lymphocyte Function-Associated Antigen-1Myeloid Differentiation Factor 88CD11a AntigenCD18 AntigensICAM1 protein, humanIntercellular Adhesion Molecule-1Interleukin-8Lymphocyte Function-Associated Antigen-1MYD88 protein, humanMyeloid Differentiation Factor 88ExosomesGenetic engineeringInflammationIntegrin aLIntegrin b2Peptide loadingTargeting

Identifiers

PMID39885580
PMCPMC11780982

What OpenQuestion holds

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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.