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Overcoming the novel glycan-lectin checkpoints in tumor microenvironments for the success of the

Mannat Jain1, Isha M Jadhav1, Suyash Vinayak Dangat1

  • 1Protein Biochemistry Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune-411033, Maharashtra, India. jainmannat193@gmail.com.

Biomaterials Science
|May 27, 2025
PubMed

Insights

Glyconanovaccines (GNVs) show promise for cancer immunotherapy by targeting C-type lectin receptors (CLRs). This review explores glycan-lectin checkpoints as novel targets to overcome resistance and enhance GNV efficacy against tumors.

Area of Science:

  • Immunology
  • Cancer Biology
  • Glycobiology

Background:

  • Glyconanovaccines (GNVs) are a promising cancer immunotherapy approach targeting C-type lectin receptors (CLRs) on dendritic cells to induce anti-cancer cytotoxic T lymphocyte responses.
  • Aberrant tumor glycosylation promotes immune evasion, posing a challenge to GNV efficacy.
  • Glycan-lectin interactions represent emerging immune checkpoints (ICs) that modulate the tumor immune landscape.

Purpose of the Study:

  • To explore glycan-lectin immune checkpoints and their impact on the efficacy of GNVs.
  • To discuss the role of altered tumor glycosylation and lectins (siglecs, galectins) in immune evasion and cancer progression.
  • To highlight current and prospective strategies for targeting glycan-lectin circuits to enhance GNVs, especially in cases of resistance to immune checkpoint inhibitors (ICIs).

Main Methods:

  • Review of existing literature on GNVs, CLRs, glycan-lectin interactions, and the tumor microenvironment (TME).
  • Analysis of the immunosuppressive mechanisms mediated by aberrant glycosylation and specific lectins within the TME.
  • Discussion of the limitations of current immune checkpoint inhibitors (ICIs) and the potential of targeting glycan-lectin circuits.

Main Results:

  • Glycan-lectin circuits function as unique immune checkpoints, influencing the effectiveness of cancer immunotherapies.
  • Siglecs and galectins contribute to an immunosuppressive TME, hindering anti-tumor immune responses.
  • Altered tumor glycosylation patterns are critical factors in immune evasion and cancer progression.

Conclusions:

  • Targeting glycan-lectin circuits offers a novel strategy to overcome resistance to existing immunotherapies and enhance GNV efficacy.
  • Understanding and manipulating glycan-lectin interactions is crucial for developing next-generation cancer immunotherapies.
  • Future research should focus on developing therapeutic approaches that modulate these circuits to fully realize the potential of GNVs.

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