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Pancreatic Cell Transplant Technique for Type 1 Diabetes

A milestone in the pursuit for a possible cure for type 1 diabetes, researchers for the Albert Einstein College of Medicine of Yeshiva University have developed a technique for transplanting insulin-producing pancreatic cells that causes only a minimal immune response in recipients.

This solves the main dilemma in cell transplantation therapy that requires patients to take immunosuppressant medication that has negative side effects. Such medication is still necessary because it inhibits the immune system from mistakenly destroying the body’s own pancreatic beta cells. These beta cells are known to produce insulin, tasked to break down sugar for body use. Without these cells there would be too much glucose in the body that can cause heart disease, kidney disease, blindness, and premature death.

Type 1 diabetes patients are burdened with monitoring their blood glucose levels and daily insulin injections for life or they can submit themselves to cellular transplantation.

However, Dr. Harris Goldstein, the study’s principal investigator, said that immunosuppressive therapy in cellular transplantation is never an assurance that the body would accept the transplanted cell. Dr. Goldstein is a professor of pediatric and of microbiology and immunology at Einstein.

To solve this, Dr. Goldstein and his colleagues experimented on the adenoviruses’ inherent capability to evade the body’s immune system. Adenoviruses are known to infect tissues that are present in the respiratory tract, intestines, eyes, and urinary tract.

The researchers observed that the infected cells reacted with adenoviruses by producing proteins that prevent the cells from informing the immune system that they have been infected and should be destroyed. In addition, the viruses are found to produce protein that is capable of shutting down the cell’s self-destruct mechanism when a foreign particle disturbs the cell’s internal function.

The effectivity of adenoviruses was tested with mice and it was noted that diabetic mice that were injected with these engineered synthetic beta cells was able to maintain glucose level for up to three months compared to the control group who showed a formal glucose control for a few days only.

“Clearly, the three proteins were not optimal, because ultimately the cells did get rejected,” said Dr. Goldstein. “We are now looking at other viral genes that also contribute to immune suppression and are trying to identify the best gene combination to use.”

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