Hands off beta cells!
Gene therapy blocks the development of an immune attack in type 1 diabetesNanonewsnet based on CFRI materials:
Gene therapy stimulates protein that blocks immune attack and prevents type 1 diabetes in mice
Activation of a specific protein in the insulin-producing region of the pancreas blocks the immune attack that causes type 1 diabetes, scientists from the Canadian Child & Family Research Institute (CFRI) report in the Journal of Clinical Investigation (Prevention of murine autoimmune diabetes by CCL22-mediated Treg recruitment to the pancreatic islets).
This discovery may eventually lead to the creation of a drug that can prevent the progression of type 1 diabetes in patients with the newly identified early stage of the disease, when the immune system has not yet had time to destroy all insulin-producing beta cells of the pancreas.
It can also help in the creation of new drugs to suppress the organ rejection reaction during transplantation and to increase the survival of transplanted islets of Langerhans – clusters of cells in the pancreas containing beta cells.
Light micrography of beta cells of the islets of Langerhans of the mammalian pancreas. Beta cells are the site of synthesis and secretion of the hormone insulin. They form clusters known as Langerhans islets. In the photo, the nuclei of beta cells are visible as dark red circles. This section is treated with monoclonal antibodies (labeled with a fluorescent dye) that bind to insulin. The yellow glow demonstrates the widespread distribution of insulin in cells, contained in numerous secretory granules that carry it to the cell membrane. (Photo: Dr. L. Orci, University of Geneva/ Science Photo Library)
Usually, when the immune system successfully copes with an infection, a special type of white blood cells - regulatory T cells (Treg) – produces chemical signals that suppress the immune response. Scientists decided to use this ability of immunity to protect beta cells from its attacks. Using a modified virus, they embedded the CCL22 protein gene into the beta cells of a genetically engineered mouse line with a diabetes model. The CCL22 protein attracts regulatory T cells that block the immune attack and protect most mice from type 1 diabetes.
The CCL22 protein was discovered many years ago in the study of ovarian cancer: scientists noticed that it is actively produced by tumors, which allows them to avoid destruction by the immune system.
"Selective shutdown of the immune system in the area of beta cells has a great advantage over the general suppression of immunity, accompanied by serious side effects," explains Dr. Bruce Verchere, professor of the Department of Pathology and Laboratory Medicine and the Department of Surgery at the University of British Columbia, lead author of the study, head of the diabetes research program in CFRI.
However, as the co-author of the work, Dr. Joel Montane, emphasizes, further research is needed before the new method can be used in the clinic.
"We need to understand this mechanism more deeply," explains Dr. Montagnier. "We don't yet know exactly how the CCL22 protein attracts regulatory T cells that suppress the immune response. Once we find the answer to this question, we may be able to develop a drug that can prevent or reverse diabetes."
"The study points to CCL22, or its modified form, as a potential drug for controlling the immune response," said Dr. Loraine Bischoff, co–author of the study. "Our strategy can be used in other autoimmune diseases, as well as in transplantology. The only difference is how to apply it."
The experimental results are doubly interesting, since regulatory T cells are currently undergoing clinical trials as a means of preventing the development of autoimmune diseases.
Portal "Eternal youth" http://vechnayamolodost.ru11.07.2011