Type 1 diabetes is an autoimmune disorder in which the immune system mistakenly attacks the body's own insulin-producing pancreatic cells, reducing and ultimately eliminating the production of insulin – a hormone needed to convert sugar, starches and other foods into energy.
Several years ago, Prof. Cohen and his colleagues developed a vaccine that arrests the progression of Type 1 diabetes in laboratory animals. They had discovered that a particular protein, called HSP60, is able to shut down the autoimmune response causing this disorder. The vaccine is currently being tested in clinical trials in Europe and the United States, but its precise mechanism has until now been unknown.
"When translating these findings into a practical vaccine, we knew enough about the mechanism to understand that this protein is able to cause a decrease in the immune response, but how it actually works eluded us," says Cohen. In a paper published in the Journal of Clinical Investigation, the scientists have managed to identify the exact immune cells that peptide p277 acts upon.
Autoimmune diseases such as type 1 diabetes occur when certain T cells in the immune system attack the body's own cells and tissues. The scientists discovered that peptide p277 directs the activity of the immune system in two ways. First, the p277 steps up the activities of a different type of T cell that regulates the amount of potentially harmful T cells. In addition, T cells treated with p277 cause the delinquent T cells to secrete anti-inflammatory substances instead of the inflammation-causing ones that they usually make. This leads to an autoimmune disease. This double action of the peptide weakens the damaging activities of the immune response further.
"These findings are important, as it means that by identifying the molecular activity of p277 with such precision, we can copy nature's own system in regulating the immune system and therefore, help to boost the immune system in preventing the destruction of insulin-producing pancreatic cells," says Cohen.
Several years ago, Prof. Cohen and his colleagues developed a vaccine that arrests the progression of Type 1 diabetes in laboratory animals. They had discovered that a particular protein, called HSP60, is able to shut down the autoimmune response causing this disorder. The vaccine is currently being tested in clinical trials in Europe and the United States, but its precise mechanism has until now been unknown.
"When translating these findings into a practical vaccine, we knew enough about the mechanism to understand that this protein is able to cause a decrease in the immune response, but how it actually works eluded us," says Cohen. In a paper published in the Journal of Clinical Investigation, the scientists have managed to identify the exact immune cells that peptide p277 acts upon.
Autoimmune diseases such as type 1 diabetes occur when certain T cells in the immune system attack the body's own cells and tissues. The scientists discovered that peptide p277 directs the activity of the immune system in two ways. First, the p277 steps up the activities of a different type of T cell that regulates the amount of potentially harmful T cells. In addition, T cells treated with p277 cause the delinquent T cells to secrete anti-inflammatory substances instead of the inflammation-causing ones that they usually make. This leads to an autoimmune disease. This double action of the peptide weakens the damaging activities of the immune response further.
"These findings are important, as it means that by identifying the molecular activity of p277 with such precision, we can copy nature's own system in regulating the immune system and therefore, help to boost the immune system in preventing the destruction of insulin-producing pancreatic cells," says Cohen.