Immunomodulation Strategies in Cancer Therapy

Immunomodulation in cancer therapy encompasses approaches that harness or redirect the patient’s own immune system to recognise and eradicate malignant cells. Central to this endeavour are strategies targeting immune checkpoints, which are inhibitory pathways exploited by tumours to evade immune surveillance. Blockade of checkpoint receptors such as PD-1 and CTLA-4 has transformed the treatment landscape for a range of solid tumours, yet response rates remain variable and toxicities can be limiting. Complementary tactics include agonism of costimulatory receptors (for example OX40, 4-1BB and GITR), which can amplify effector T-cell activation and memory formation. In parallel, depletion or functional reprogramming of immunosuppressive elements in the tumour microenvironment – notably regulatory T cells and myeloid-derived suppressor cells – can restore antitumour immunity. Antibody engineering has refined target selectivity and Fc-mediated effector functions, while adoptive cell therapies and personalised cancer vaccines harness antigen specificity to bolster cytotoxic responses. Synthetic biology and in silico models offer increasingly sophisticated tools to predict and optimise combination regimens. Taken together, these interlinked modalities promise to overcome resistance mechanisms, broaden the cohort of responders and deliver durable control of diverse malignancies.

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Immunomodulation Strategies in Cancer Therapy publication trend

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Technical terms

Immune checkpoint: An inhibitory receptor-ligand pathway that regulates T-cell activation and maintains self-tolerance, often co-opted by tumours to suppress antitumour responses.

Costimulatory receptor: A cell-surface molecule (for example OX40, 4-1BB, GITR) that delivers activating signals to T cells upon ligand engagement, enhancing proliferation and effector functions.

Regulatory T cell: A subset of CD4+ T cells characterised by expression of FOXP3 that suppresses immune activation and maintains tolerance, but can be co-opted by tumours to evade immunity.

Myeloid-derived suppressor cell: A heterogeneous population of immature myeloid cells that accumulate in the tumour microenvironment and inhibit T-cell function via soluble mediators and cell-cell contact.

Tumour microenvironment (TME): The complex milieu surrounding a tumour, including stromal cells, immune infiltrates, extracellular matrix and soluble factors that collectively influence tumour progression and therapeutic response.

References

1. Engineering antibodies with cancer‐associated binding sites. BMEMat (2024).
2. Quantitative Approach to Explore Regulatory T Cell Activity in Immuno-Oncology. Pharmaceutics (2024).
3. Expression patterns of novel immunotherapy targets in intermediate- and high-grade lung neuroendocrine neoplasms. Cancer Immunology, Immunotherapy (2024).
4. Immune checkpoint blockade and its combination therapy with small-molecule inhibitors for cancer treatment. Biochimica et Biophysica Acta (BBA) - Reviews on Cancer (2018).