Scientists and colleagues at the van Endal Institute have discovered a possible treatment target that can re -activate the immune cells in their fight against cancer.

The target is an immune checkpoint called PTGIR, which controls the number and cancer -fighting powers. T cellsSoldiers of the immune system. Ptgir puts a break on the Ptgir T cells and reduces their ability to release cancer-killing molecules.

Conclusion, published in magazine Nature of natureNew immune checkpoint inhibitors or engineer T can help improve cancer immunotherapy by paving the way for T cell therapy that reappears PTGIR signaling and T cells.

Immunotherapy is a game changer for the treatment of cancer, but they do not work for everyone or for all cancer. Blocking PTGIR provides another opportunity to develop more targeted treatment that helps fight the immune system. ,

Michael Dahebih, PhD, first writer of study and in PostDoctorl Fellow, PhD, VA in Russell Jones laboratory.

There are molecules of immune posts that contain black pepper outside T cells and some cancer cells. In immune cells, the outposts helped the immune system to do their work without accidentally attacking healthy cells. In cancer, posts allow malignant cells to avoid immune attacks. Medications that block the posts called immune checkpoint inhibitors have become a powerful tool for the treatment of cancer.

Most known immune posts depend on interaction between proteins, which can limit treatment options. The new checkpoint is based on a protein (PTGIR) and a lipid (prostaclin), which creates new possibilities to take advantage of the checkpoint to fight cancer. To date, only a few similar protein-lipid interactions in T cells have been described.

Prostisclin is found in and around in the tumor and contributes to T cell tiredness by interacting with PTGIR. The amount and availability of PTGIR are regulated by another protein called NRF2. More NRF2 means more PTGIR – resulting in broad T cell tiredness.

Jones said, “The more PTGIR, the more opportunities are there for it to interact with prostisclin.” “This enlarged activity slams the brake on T cell activity and continue to fight cancer cells makes them more difficult for them. Closing this interaction gives an opportunity to increase the immune system and treat cancer.”