Since 2007, we at New Hope Unlimited have been using Immunotherapy very successfully. However, the way we do our immunotherapy protocols are very different than the way the United Staes medical teams do their protocols. Our process is done by using the patient’s own blood and only natural agents to expand the immune cells. The US is still trying to do the process by using synthetic agents. The following article is reporting information on the United States’ way of doing things.
The University of Pittsburgh School of Medicine and UPMC researchers have discovered a clue that might unlock the potential of immunotherapy drugs that will successfully treat more cancers. The magazine Cell published the findings that showed targeting a sub-population of immune cells called regulatory T cells (Tregs) could be an effective approach to treating cancers, as shown in their study of mice. This might also be an important mechanism by which current immunotherapy drugs work and provide clues to make them more effective.
The current immunotherapy drugs that push the immune system to kill cancer cells have been successful against several of the cancers, but are still only effective in about 10 to 30% of those with certain tumor types. It has remained a mystery why these drugs don’t work in more patients and this discovery points to what could be an important mechanism how current immunotherapy drugs work and provide clues to making them more effective.
Our immune system uses Tregs to help maintain a delicate balance. It’s kind of like a dimmer switch where keeping the light bright enough to detect and eliminate threats works, but not so bright that our own cells are hurt, according to Dario Vignali, Ph.D., who holds the Frank Dixon Chair in Cancer Immunology. He is also professor and vice chair of immunology at Pitt’s School of Medicine and co-director of the Cancer Immunology Program at the UPMC Hillman Cancer Center.
Tregs can be detrimental as turning down the lights in cancer causes them to prevent the immune system from detecting and killing the cancer cells. There could be life threatening autoimmune complications by eliminating Tregs and making them unusable in cancer patients. Therefore, it is necessary to identify approaches that selectively target Tregs in tumors and spare those outside the tumor.
Vignali and his colleagues discovered previously that a surface protein called neuropilin-1 (Nrp1) is expressed on almost all Tregs that infiltrated mouse tumors and was required to maintain the function, integrity and survival of Tregs within the harsh tumor microenvironment. So Nrp1 on Tregs does help suppress the body’s natural anti-tumor immune response and helps the tumor survive. By blocking or deleting Nrp1 in Tregs in mice, it only impacted their function in tumors and not the rest of the body, resulting in tumor eradication without inducing autoimmune or inflammatory disease.
They have shown in this study of mice that Nrp1 expression by Tregs is required to maintain their ability to prevent the immune system from clearing the tumor. A genetically modified mouse model was created in which the Nrp1 gene was deleted in only ½ of the Treg cell population and not the other ½. The tumor growth in this model was found dramatically reduced when compared to a normal mouse in which Nrp1 was present in all Tregs.
Not only did they have a reduced ability to turn down the lights but they also prevented the normal Treg population from performing their own immunosuppressive functions, allowing the immune system to see and attack the tumor. The analyses revealed a secreted immune molecule called interferon-gamma (IFNy) that prevented the dimmer switch function of Tregs in mice, especially in the tumor microenvironment.
The authors believe their findings are significant because they have shown that if we can get a portion of the tumor-associated Tregs to lose their immunosuppressive function it may be enough to set off a chain reaction where the cells cans influence other tumor-associated Tregs.
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