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Immunotherapy and Immune Responses / Immune Cells in Cancer · Journal article
Frontiers in Immunology · September 8, 2026
Raises a question worth testing. It does not answer one.
This narrative review examines how transmembrane lectins (C-type lectin receptors and Siglecs) on myeloid cells recognise altered cancer glycans and transduce immunosuppressive signals. The authors integrate mechanistic evidence from glycobiology and immunology to propose these receptors as therapeutic targets but acknowledge substantial complexity—receptor redundancy, overlapping ligand specificities, and context-dependence—that complicates translation. No new empirical data or clinical outcomes are reported.
Journal article. Cancer cells and the tumor microenvironment; myeloid populations (macrophages, dendritic cells) and their immunosuppressive interactions with malignant and stromal cells..
Transmembrane lectins on myeloid cells couple glycan recognition to signaling that regulates macrophage and dendritic-cell states, antigen presentation, phagocytosis, cytokine production, metabolism, and immune-checkpoint regulation. Altered glycosylation is a recurrent feature of cancer that reshapes ligands available to lectin receptors. Receptor redundancy, overlapping glycan specificities, and model-dependent effects complicate interpretation and therapeutic targeting of lectin pathways.
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This review identifies transmembrane lectins as potential therapeutic targets for reversing myeloid-mediated immunosuppression in cancer. Clinicians and drug developers should note that the complexity of lectin biology—redundancy and context-dependence—suggests single-target inhibition may be insufficient; combinatorial or glycan-directed approaches may be needed.
A narrative review synthesizing mechanistic concepts and therapeutic potential of lectin–glycan interactions in cancer immunity, raising questions rather than reporting empirical results or clinical outcomes.
This review identifies transmembrane lectins as potential therapeutic targets for reversing myeloid-mediated immunosuppression in cancer. Clinicians and drug developers should note that the complexity of lectin biology—redundancy and context-dependence—suggests single-target inhibition may be insufficient; combinatorial or glycan-directed approaches may be needed.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Immune evasion in cancer is sustained by coordinated interactions between malignant, stromal, and immune cells within the tumor microenvironment. Among these, myeloid populations are major regulators of immunosuppression, but the diverse signals that shape their functional states remain insufficiently integrated within current conceptual frameworks. Altered glycosylation is a recurrent feature of cancer that reshapes the ligands available to lectin receptors. Within this landscape, transmembrane lectins expressed by myeloid cells occupy a distinctive mechanistic position, coupling extracellular glycan recognition to intracellular signaling programs that shape myeloid-cell function. In this review, we integrate evidence from tumor glycobiology, myeloid immunology, receptor signaling, experimental models, and therapeutic development to examine how C-type lectin receptors and Siglecs contribute to myeloid-mediated immune suppression. We discuss how these receptors influence macrophage and dendritic-cell states, antigen presentation, phagocytosis, cytokine production, metabolism, and immune-checkpoint regulation, while emphasizing the dependence of these outcomes on ligand context, receptor architecture, cellular identity, and tissue organization. We further consider how receptor redundancy, overlapping glycan specificities, and model-dependent effects complicate the interpretation and therapeutic targeting of lectin pathways. Finally, we discuss emerging approaches directed at lectin–glycan interactions and downstream signaling, together with their potential to complement established immunotherapies. By bringing together concepts that are often considered separately, this review positions transmembrane lectins as important integrators of the tumor glycan landscape and myeloid immune regulation, while defining key questions that must be addressed to translate glyco-immune mechanisms into effective cancer therapies.
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