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This research aims to uncover the regulatory mechanisms of CD47 and identify new immune checkpoints in Acute Myeloid Leukemia (AML).

December 8, 2025BloodOpen Access

CD43 functions as a CD47 independent “don't eat me” signal and novel immune checkpoint in AML

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This research aims to uncover the regulatory mechanisms of CD47 and identify new immune checkpoints in Acute Myeloid Leukemia (AML).
Performed genome-wide CRISPR knockout screens in AML cell lines MOLM13 and U937.
Investigated the role of O-glycosylation and fucosylation in regulating CD47 using genetic deletions and inhibitors.
Analyzed phagocytosis levels with and without CD43 blockade in AML cells.
Identified CD43 as an O-glycosylated molecule that negatively regulates CD47 expression.
Demonstrated that deletion of CD43 increased macrophage phagocytosis in AML cells by threefold.
Found that elevated CD43 expression correlates with poor overall survival in AML patients.

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Genome-wide CRISPR screens identified CD43's role in phagocytosis in AML, suggesting it as a target for immunotherapy.

Wang et al. (2025) studied this question.

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