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Weakened macrophage antibacterial capacity in myelodysplastic syndrome.

Created on 18 Jul 2026

Authors

Johnathon B Schafer, Kenneth C Malcolm, Jessica Dell-Martin, Maria L Amaya, Daniel A Pollyea, Scott Alper

Published in

ImmunoHorizons. Volume 10. Issue 7. Jul 10, 2026.

Abstract

Patients with myelodysplastic syndrome (MDS) are immunocompromised and are therefore susceptible to fatal infection. While neutropenia and neutrophil dysfunction account for much of this immunodeficiency, other immune cells likely also contribute. In contrast to the extensive study of neutrophils in MDS, there has been very little investigation of macrophage host defense function in MDS. In the current study, we find that macrophage differentiation and macrophage phagocytosis of bacteria are greatly weakened in patients with MDS, regardless of patient genotype. Moreover, we find that killing of those bacteria that are ingested is diminished in MDS patients with high-risk disease. Using a mouse model that expresses the MDS-associated U2AF1-S34F mutation, we find that this mutation is sufficient to induce macrophage functional defects. We conclude that macrophage host defense defects likely contribute to the immunodeficiency present in MDS.

PMID:
42467566
Bibliographic data and abstract were imported from PubMed on 18 Jul 2026.

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