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December 8, 2025Blood0 citationsOpen Access

CD43: A Novel Immune Checkpoint Independent of CD47 in Acute Myeloid Leukemia

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

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Authors

CWChuqi WangJSJavier Sanmartín-MartínezSJShaista Jasdanwala

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Overview

Genome-wide CRISPR screening reveals CD43 as an immune checkpoint in AML, implicating therapies targeting fucosylation may improve phagocytosis.

Key Points

  • This research aims to investigate CD43 as a novel immune checkpoint that functions independently of CD47 in acute myeloid leukemia (AML).
  • Performed genome-wide CRISPR knock-out screens in AML cell lines MOLM13 and U937.
  • Identified genes influencing CD47 levels related to O-glycosylation and fucosylation.
  • Utilized inhibitors of O-glycosylation to investigate their effects on CD47 expression.
  • Conducted Kaplan-Meier survival analysis on AML patients to assess CD43's impact on overall survival.
  • Deletion of O-glycosylation-modifying genes increased CD47 and phagocytosis in AML cell lines.
  • Inhibition of fucosylation decreased CD47 levels and binding to SIRPa-Fc.
  • Elevated CD43 expression correlated with worse overall survival in AML patients.
  • CD43 was identified as a novel immune checkpoint promoting an immunosuppressive environment in AML.
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Cite This Study

Wang et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d108https://doi.org/10.1182/blood-2025-5025
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