ercent of the study samples by either slowing or stopping the progression of breast cancer. In at least one case, the vaccine worked for as long as 39 weeks.
Because the use of synthetic peptides alone generally does not trigger a strong immune response, researchers administered the vaccine in combination with a Toll-like receptor stimulant that is designed to mimic the way in which an invading bacterial agent would induce an immune response in humans.
Under normal conditions, the response is generally strong enough for the body to recognize and attack invading bacteria. Researchers used this strategy, but also introduced anti-CD25 antibodies to increase the immune response. These antibodies control the production of T regulatory cells that can prevent the vaccine from doing its job, but by combining the two strategies (immunization and depletion of T regulatory mechanisms), the vaccine successfully passed through the T cell checkpoint. This approach was successful in stimulating an effective immune response.
"We found that we could train the immune system to recognize these synthetic peptides as dangerous foreign agents of the HER-2/neu gene by mimicking what the bacteria would do in your body. The body responded by killing everything that expressed HER-2/neu in high amounts," Dr. Nava-Parada said. In addition, "we estimate that in a real life scenario, we could probably use this technique to decrease the number of immunizations a patient would need (one instead of three), to build an immune response strong enough to destroy the tumor."
Dr. Nava-Parada said that up until now, researchers undertaking similar work have only been able to get vaccines to work in about 30 percent of HER-2/neu study models, but only by depleting T regulatory cells, which can have negative side effects, such as an autoimmune disorder. "In our study we showed that we can prevent tumors without depleting these cells and can achieve this succes
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