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Tumor Immunotherapy01:27

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Glycoengineering CAR-T cells to overcome galectin-3-mediated immunosuppression.

Lee Seng Lau1, Maria Suarez1, Brandon Fernandez1

  • 1Department of Cellular and Molecular Medicine, Herbert Wertheim College of Medicine, Florida International University, Miami, FL, United States.

Frontiers in Immunology
|March 6, 2026
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Summary
This summary is machine-generated.

Chimeric antigen receptor (CAR)-T cell therapy shows promise but faces challenges. Enhancing ST6GAL1 expression in CAR-T cells improves their persistence and anti-tumor activity by reducing immunosuppression from galectin-3.

Keywords:
CAR-T cellscancer glycobiologycancer immunotherapygalectinssialylation modification

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Area of Science:

  • Immunology
  • Cell Therapy
  • Glycobiology

Background:

  • CAR-T cell therapy is effective for B-cell malignancies but limited by persistence and toxicity.
  • T cell function is influenced by glycan signatures and galectin interactions.
  • CAR-T cells may possess glycan features making them vulnerable to immunosuppressive galectins.

Purpose of the Study:

  • To investigate the role of galectin-3 in CAR-T cell function.
  • To determine if CAR-T cells exhibit galectin-3 binding glycans and reduced ST6GAL1 expression.
  • To explore targeted sialylation as a strategy to enhance CAR-T cell efficacy.

Main Methods:

  • Public data mining, glycomics, and assessment of galectin-binding and glycosyltransferase expression.
  • Analysis of anti-CD19 CAR-T cells and lymphoma-associated microenvironments.
  • Genetic enforcement of ST6GAL1 expression in CAR-T cells.

Main Results:

  • Galectin-3 was elevated in lymphoma microenvironments; CAR-T cells showed increased Gal-3-binding glycans and reduced ST6GAL1.
  • Enforcing ST6GAL1 in CAR-T cells blocked Gal-3 binding and reversed Gal-3-mediated immunosuppression.
  • ST6GAL1-enhanced CAR-T cells maintained tumoricidal activity, improved anti-tumor responses, and showed increased in vivo persistence.

Conclusions:

  • Galectin-3 is a significant extrinsic suppressor of CAR-T cell function.
  • Targeted cell surface α2,6 sialylation via ST6GAL1 is a viable strategy to improve CAR-T cell resistance.
  • This approach enhances CAR-T cell persistence and anti-tumor efficacy in immunosuppressive environments.