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July 24, 2018
The importance of the EPA enzyme as a key regulation of the immune system has been discovered in new research from the University of Newcastle, UK.
Factors that regulate the immune system play a key role in keeping the immune system in balance. Too active and there is a risk of developing autoimmune diseases such as rheumatoid arthritis. The cells and the infections too pbadive and cancerous are free to develop. A key regulator is the inhibitory co-receptor PD-1. Antibodies to this co-receptor, known as checkpoint inhibitors, have successfully activated the immune system to attack cancer cells, although their responses are not always successful or long-lasting .
Today, researchers led by Dr. Shoba Amarnath have studied the factors that were inhibited by the activation of PD-1 in immune cells. One such factor was the enzyme AEP. In the absence of PEA, the mice were resistant to autoimmune diseases but sensitive to tumor cells.
Dr. Amarnath explains, "What we found in our laboratory studies is that EPA improves the effect of these checkpoint inhibitors in advanced melanoma.
"When it was at higher levels in immune system T cells, the PEA support worked in combination with the checkpoint inhibitor drug in many diseases. He has successfully attacked tumors in skin cancer, activating the immune system and preventing host disease by deactivating the immune system.
"Remarkably, while we have known about the existence of EPA, we have not until now understood how important it is to help the immune system fight a certain number of diseases. "
As PD-1 inhibitors need EPA to improve immune responses, measurement of EPA levels may help identify the most likely patients with inhibitor therapy Immune Control Point to PD1 and PDL1.
Understanding Why Checkpoint Inhibitors Work
The Research Team Led by Dr. Amarnath Identified How Immune Cells Affect Inactive tumors in the tumor microenvironment CD4 + helper T cells are a type of immune cell that recognizes and kills infected cells and cancer cells. autoimmune ladie and rejection of the graft. Because these cells can kill healthy tissue, their activity is tightly controlled by another type of immune cell known as regulatory T cells.
It has been suggested that the protective activity of regulatory T cells interferes with the treatments of immunotherapy. The local environment of some tumors enhances the formation of regulatory T cells which in turn limits the activation of T cells.
When Dr. Amarnath's team investigated how PD-1 was blocking these cancerous cells; they found that PD-1 specifically regulated a new enzyme called asparaginyl endopeptidase (AEP), which was essential to alter the balance between cancer cells and regulatory T cells in the melanotic tumor environment.
These results demonstrate that checkpoint inhibitors a beneficial response in the absence of PEA and measurement of EPA protein levels in patients prior to treatment with checkpoint inhibitors may provide better rates. of response to cancer immunotherapy regimens. Similarly, in mice, when the researchers activated PD-1 signaling in T-cells and blocked EPA, potent T regulatory cells were generated to prevent inflammatory diseases such as colitis and Parkinson's disease. graft against the host. This discovery may be able to generate new immunotherapy treatments for patients who do not currently respond to standard regimens for colitis and graft versus host.
The Newcastle team now has the intention of advancing humans.
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