Journal
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY
Volume 86, Issue 9, Pages 1726-1735Publisher
WILEY
DOI: 10.1111/bcp.14351
Keywords
damage-associated molecular patterns; dendritic cells; immunotherapy; innate and adaptive immunity; myeloid-derived suppressor cells; natural killer cells; radiation therapy; tumour-associated macrophages
Categories
Funding
- CRUK City of London Centre [C7893/A26233]
- CRUK Clinical Research Training Fellowships [549580]
- CRUK National Cancer Imaging Translational Accelerator [C1519/28682, C604/A25135]
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Radiation therapy is an essential component of cancer care, contributing up to 40% of curative cancer treatment regimens. It creates DNA double-strand breaks causing cell death in highly replicating tumour cells. However, tumours can develop acquired resistance to therapy. The efficiency of radiation treatment has been increased by means of combining it with other approaches such as chemotherapy, molecule-targeted therapies and, in recent years, immunotherapy (IT). Cancer-cell apoptosis after radiation treatment causes an immunological reaction that contributes to eradicating the tumour via antigen presentation and subsequent T-cell activation. By contrast, radiotherapy also contributes to the formation of an immunosuppressive environment that hinders the efficacy of the therapy. Innate immune cells from myeloid and lymphoid origin show a very active role in both acquired resistance and antitumourigenic mechanisms. Therefore, many efforts are being made in order to reach a better understanding of the innate immunity reactions after radiation therapy (RT) and the design of new combinatorial IT strategies focused in these particular populations.
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