Immunotherapy is a type of cancer treatment that uses your own immune system to help fight cancer. Stimulating a patient’s own immune system can be highly effective at recognizing and destroying cancer cells. Programmed death-ligand 1 (PD-L1) is a transmembrane protein that can suppress the immune response by inhibiting the proliferation of T cells via apoptosis. It also plays an important role in arresting cell-cycle progression. Normally, the immune system will detect foreign antigens and trigger the proliferation of the immune response including T cells. The binding of programmed cell death-1 (PD-1) to PD-L1 reduces the proliferation of the T cells. PD1/PD-L1 interaction ensures that activation of the immune system occurs at the appropriate time and to minimize the possibility of chronic autoimmune inflammation.
Unfortunately, upregulation of PD-L1 may allow cancers to evade the immune response. Many immune-oncology therapies use PD-L1 inhibitors with great success. PD-1 can trick your immune system into overlooking cancer cells as normal cells. Recently, a new report identified another protein, CMTM6, which stabilizes PD-L1 and increases the ability of cancer cells to avoid being destroyed by inhibiting the immune response. CMTM6 was identified using a genome-wide CRISPR–Cas9 screen. CMTM6 co-localizes with PD-L1 at the plasma membrane and in endosomes, where it prevents PD-L1 from being degraded. Interestingly, interfering with CMTM6 expression impairs PD-L1 protein expression. Therefore, this makes CMTM6 an attractive therapeutic target for cancer and immunologic diseases.
For more information:
https://www.ncbi.nlm.nih.gov/labs/articles/28813417/
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