Evidence map›Paper›PMID 28878781›Full record

ArticleFrontiers in immunology2017

Calreticulin Release at an Early Stage of Death Modulates the Clearance by Macrophages of Apoptotic Cells.

Rim Osman, Pascale Tacnet-Delorme, Jean-Philippe Kleman, Arnaud Millet, Philippe Frachet

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Macrophages release neuraminidase and cleaved calreticulin for programmed cell removal.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Review
  6. Article
  7. Frontiers in immunology · 2025
    Article
  8. Review
  9. Review
  10. The Role of Extracellular Vesicles in Efferocytosis.Mini reviews in medicinal chemistry · 2024
    Review
  11. Article
  12. Calreticulin as a marker and therapeutic target for cancer.Clinical and experimental medicine · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

Rim OsmanUniversity Grenoble Alpes, Institut de Biologie Structurale (IBS), CNRS, CEA, Immune Response to Pathogens and Altered Self (IRPAS) Group, Grenoble, France.
Pascale Tacnet-DelormeUniversity Grenoble Alpes, Institut de Biologie Structurale (IBS), CNRS, CEA, Immune Response to Pathogens and Altered Self (IRPAS) Group, Grenoble, France.
Jean-Philippe KlemanUniversity Grenoble Alpes, Institut de Biologie Structurale (IBS), CNRS, CEA, Immune Response to Pathogens and Altered Self (IRPAS) Group, Grenoble, France.
Arnaud MilletATIP/Avenir Team Mechanobiology, Immunity and Cancer INSERM U1205, Université Grenoble Alpes, Grenoble, France.
Philippe FrachetUniversity Grenoble Alpes, Institut de Biologie Structurale (IBS), CNRS, CEA, Immune Response to Pathogens and Altered Self (IRPAS) Group, Grenoble, France.
Centre National de la Recherche Scientifique · FRInstitut de Biologie Structurale · FRImmunité et Cancer · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calreticulin (CRT) is a well-known "eat-me" signal harbored by dying cells participating in their recognition by phagocytes. CRT is also recognized to deeply impact the immune response to altered self-cells. In this study, we focus on the role of the newly exposed CRT following cell death induction. We show that if CRT increases at the outer face of the plasma membrane and is well recognized by C1q even when phosphatidylserine is not yet detected, CRT is also released in the surrounding milieu and is able to interact with phagocytes. We observed that exogenous CRT is endocytosed by THP1 macrophages through macropinocytosis and that internalization is associated with a particular phenotype characterized by an increase of cell spreading and migration, an upregulation of CD14, an increase of interleukin-8 release, and a decrease of early apoptotic cell uptake. Importantly, CRT-induced pro-inflammatory phenotype was confirmed on human monocytes-derived macrophages by the overexpression of CD40 and CD274, and we found that monocyte-derived macrophages exposed to CRT display a peculiar polarization notably associated with a downregulation of the histocompatibility complex of class II molecules hampering its description through the classical M1/M2 dichotomy. Altogether our results highlight the role of soluble CRT with strong possible consequences on the macrophage-mediated immune response to dying cell.

Indexed as

apoptotic cellsC1qcalreticulinCD14efferocytosismacrophage polarization

Identifiers

PMID28878781
PMCPMC5572343
OpenAlexW2746715991

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.