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Updated: May 10, 2026

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Published on: December 3, 2020
CD47 in Erythrocyte Ageing and Clearance - the Dutch Point of View
Patrick Burger1, Dirk de Korte, Timo K van den Berg
1Sanquin Research and Landsteiner Laboratory, Academic Medical Centre, University of Amsterdam, the Netherlands.
Insights
CD47, a
Area of Science:
- Immunology and Cell Biology
- Hematology
Background:
- CD47 acts as a 'don't eat me' signal, inhibiting phagocytosis.
- Aged erythrocytes are typically cleared via CD47-mediated signaling.
- Recent findings suggest CD47 can switch to an 'eat me' signal.
Purpose of the Study:
- To review molecular mechanisms of CD47 conformational change.
- To discuss signal transduction in CD47-mediated erythrocyte phagocytosis.
- To address consequences for aged erythrocyte clearance and transfusion.
Main Methods:
- Review of experimental data and literature.
- Analysis of molecular pathways involved in CD47 signaling.
- Discussion of cellular mechanisms of phagocytosis.
Main Results:
- CD47 can undergo a conformational change, converting its signal from 'don't eat me' to 'eat me'.
- This switch appears to involve the same receptor, SIRPα, which normally inhibits phagocytosis.
- This mechanism impacts aged erythrocyte clearance and post-transfusion outcomes.
Conclusions:
- The CD47 'eat me' signal switch is a novel mechanism for erythrocyte clearance.
- Understanding this pathway is crucial for managing erythrocyte turnover and transfusion efficacy.
- Further research into CD47 modulation could offer therapeutic strategies.
Abstract:
Recently, an important role for CD47, a well-known 'don't eat me' signal, in the clearance of aged erythrocytes was revealed. Experimental data support the conversion of CD47 from a 'don't eat me' to an 'eat me' signal through a conformational change in CD47. Intriguingly, erythrocyte phagocytosis after this switch seems to be mediated by the same receptor that normally signals inhibition of phagocytosis, SIRPα. In this review, the possible molecular mechanisms leading to this conformational change in CD47 as well as the possible signal transduction events leading to phagocytosis after this switch are discussed. Lastly, the consequences of this newly identified mode of erythrocyte phagocytosis for the clearance of aged erythrocytes during normal turnover and after erythrocyte transfusion are addressed.
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The resident phagocytic macrophages deal with these damaged cells by engulfing them and separating their globin and heme groups.

