Hematology · Oncology · 2 h ago
CD24-directed therapies counter CD19 CAR-T resistance in preclinical B-cell malignancy models
A preclinical study in Leukemia evaluated CD24-directed antibodies and engineered T cells in lymphoma and leukemia models. Researchers reported activity against CD19 CAR-T resistance associated with antigen loss and apoptosis defects, alongside enhanced macrophage-mediated clearance; clinical efficacy and safety remain unestablished.
- CD24-directed approaches showed activity in resistant lymphoma and leukemia models.
- Targeted T cells enhanced macrophage-mediated phagocytic clearance.
- Dual CD19/CD24 targeting showed improved preclinical efficacy.
- Clinical benefit and safety remain unestablished.
Researchers investigated CD24 targeting as a strategy to address resistance to CD19 chimeric antigen receptor T-cell (CAR-T) therapy in B-cell malignancies. The preclinical study evaluated a CD24 × CD3 bispecific antibody and CXCR3-armed CD24 CAR-T cells in lymphoma and leukemia models, using in vitro and in vivo experiments.
Both approaches showed antitumor activity in models with CD19 CAR-T resistance driven by antigen loss or apoptosis defects. CD24-targeted T cells also shifted macrophages toward an M1-like phenotype and enhanced phagocytic clearance. The investigators additionally engineered CD19 CAR-T cells that secrete a CD24 bispecific T-cell engager, reporting improved efficacy with simultaneous CD19 and CD24 targeting.
These findings support further investigation of CD24-directed strategies for resistant B-cell malignancies, but do not establish benefit in patients. The supplied abstract provides no sample sizes, quantitative effect estimates, or safety results, limiting assessment of the magnitude and translational relevance of the findings.
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Leukemia: Combating CD24 to overcome CD19 CAR-T resistance via induction of innate and adaptive immunity in B-cell malignancies ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.