Immune Cells and the Link to Immunotherapy
Immunotherapy has been around for quite some time, and it’s one of the therapies in the fight against cancer that could change the way we look at cancer treatment. However, even the most successful treatments still face an uphill battle when it comes to the intricacies of cancer. Immunotherapy is successful in about 10-30% of cancer patients with specific types of tumors. Even some of the more aggressive cancers have been treated with immunotherapy simply based on the type of tumor that has been growing. For a long time now, no one has been able to answer why exactly the number has remained so low, but researchers at University of Pittsburgh School of Medicine and UPMC may have found a clue that could unlock the power of immunotherapy drugs and raise their success rates.
Regulatory T cells are an important cell in our bodies, often alerting our bodies to threats and yet maintaining a balance so as to not harm other cells in those alerts. When we have cancer, our T cells end up not functioning and alerting us of threats. Basically, the T cells malfunction and don’t allow the immune system to identify cancerous cells and eliminating them. Removing the T cells may sound like a logical treatment, but it leaves us with an autoimmune deficiency that would open us up to other cancers and diseases. Thus, targeting t cells within the tumor (those that are malfunctioning), is a far better approach for successful treatment.
Studies in mice have revealed a protein, called neuropilin-1 (Nrp1), that exist on T Cells in the harsh tumor environment. When the protein is expressed from T cells, the T cell is able to become active participants in the anti-tumor response. Meaning that if we remove the protein, the immunotherapy may work at a higher success rate. To discover this, the researchers created a mice module with half of their mice owning the protein (the normal mouse) and the other having had it expressed (abnormal mouse). Tumor growth in the abnormal mouse was significantly reduced when compared with the normal mouse. The lack of protein in the abnormal mouse allowed the immune system to attack the tumor without intervention of the protein-rich T cell.
This is an impressive step in our fight against various cancers. If we are able to get a portion of the tumor-associated T cells to lose their immunosuppressive functions, we could set off a chain reaction where the cells trigger other tumor-associated T cells and promote anti-tumor immunity without the adverse autoimmune side effects we have seen previously. We will have to watch this progress as it makes it way to human subjects to – hopefully – see major growth in our fight against cancer.