What is it about?

Inosine pranobex (IP) is licensed as an antiviral drug. It's mechanism of action is incompletely understood. Our paper shows that exposing cancer cell lines to inosine pranobex makes the cancer cells more recognisable to the immune system, and more susceptible to immune cell-mediated killing. This effect is explained by IP-induced increased expression of NKG2D ligands at the cell surface, and triggering of NKG2D receptor activation on immune cells. Activation of NKG2D signalling on immune cells (including NK cells, NKT cells, gamma delta T cells and CD8+ T cells) is known to promote direct cellular cytotoxicity, cytokine secretion, or co-stimulation, depending on the immune context.

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Why is it important?

Fine-tuning the immune system's response to cancer cells has underpinned many recent advances in cancer therapy. Understanding the molecular mechanisms that control immune responses, and how to modify these mechanisms can help to design better cancer treatments in the future.

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This page is a summary of: Inosine pranobex enhances human NK cell cytotoxicity by inducing metabolic activation and NKG2D ligand expression, European Journal of Immunology, August 2019, Wiley,
DOI: 10.1002/eji.201847948.
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