Toll-Like Receptor Modulation in Cancer Immunology
Summary
Toll-like receptors (TLRs) serve as pivotal sentinels of the innate immune system, recognising pathogen- and damage-associated molecular patterns to initiate inflammatory and adaptive immune responses. In cancer, TLRs expressed on tumour cells, antigen-presenting cells and stromal components can exert dichotomous roles, either promoting anti-tumour immunity or fostering a protumour microenvironment through chronic inflammation and immunosuppression. Modulation of TLR signalling—via agonists to enhance dendritic cell maturation and cytotoxic T-cell activation, or via antagonists to attenuate tumour-promoting inflammation—has emerged as a versatile strategy in immuno-oncology. Advances in structural biology and ligand design have enabled the development of synthetic agonists, small-molecule inhibitors and targeted delivery systems that reshape the tumour microenvironment, synergise with checkpoint blockade and improve the efficacy of conventional therapies. As our understanding of TLR-driven cross-talk between innate and adaptive immunity deepens, so too does the prospect of precise, context-dependent interventions that harness or restrain TLR pathways for clinical benefit.
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Toll-Like Receptor Modulation in Cancer Immunology publication trend
The graph below shows the total number of articles in toll-like receptor modulation in cancer immunology across all publications each year (not limited to Nature Index journals).
Technical terms
Toll-Like Receptors (TLRs): A family of innate immune receptors that detect pathogen-associated or damage-associated molecular patterns to initiate inflammatory responses.
Pattern Recognition Receptors (PRRs): Receptors expressed on innate immune cells that recognise conserved molecular motifs of pathogens or injured cells.
Adaptor Protein MyD88: A key intracellular signalling molecule that bridges TLR activation to downstream cascades leading to cytokine production.
Epithelial–Mesenchymal Transition (EMT): A cellular process by which epithelial cells acquire motility and invasiveness, facilitating cancer metastasis.
Tumour Microenvironment (TME): The complex cellular and molecular milieu surrounding a tumour, comprising immune cells, stromal cells and signalling factors.
References
- Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives. Frontiers in Immunology (2023).
- Robinin inhibits pancreatic cancer cell proliferation, EMT and inflammation via regulating TLR2-PI3k-AKT signaling pathway. Cancer Cell International (2023).
- Toll-like receptors activation, signaling, and targeting: an overview. Bulletin of the National Research Centre (2019).
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