Who Are Those Masked Cells? They’re Researchers’ Answer to Avoiding Transplant Rejection

On the research front

Dec 2, 2008

One of the most promising approaches to the treatment of type 1 diabetes is the transplantation of human islet cells. The major drawback to the procedure has been that even though recipients initially enjoy revitalized pancreases that pump out copious amounts of insulin, their immune systems soon act as spoilsports and reject the donated cells. 

Currently, the only way around the problem is to give patients powerful drugs that suppress their immune responses. Unfortunately, the drugs themselves can harm the newly transplanted cells, as well as leave patients exposed to infections.

But an artful solution may be on the way. Working with diabetic mice, researchers at Northwestern University's Feinberg School of Medicine have succeeded in tricking the animals' immune systems into perceiving transplanted islet cells as their own. As a result, the cells continue to thrive-a far cry from their average 15-day lifespan after normal transplant procedures.

What the researchers did was to take splenocytes, a type of white blood cell, from the donor's spleen and treat them with a chemical that masked their identity. They injected the cells into diabetic mice before and after the mice underwent islet cell transplantation. When the actual islet cells were transplanted, the mouse immune systems did not sense them as foreign or dangerous and therefore did not reject them.

In more than 70 percent of the mice that received the treated splenocytes, the transplanted islet cells thrived for at least 150 days.

The next step will be to see if the same technique can be applied to treat autoimmune disease itself, "tricking" mice that are prone to acquiring diabetes into ceasing the attacks on their own bodies that destroy their insulin-making powers. 

If that step is successful, the cell therapy will be tested on human subjects.

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Categories: Diabetes, Diabetes, Insulin, Islet & Pancreas Transplant, Research, Type 1 Issues

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Dec 2, 2008

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