I do not like vaccinations. I wonder if they are connected to the autism and diabetes epidemics, even attention-deficit disorders. I do vaccinate my children, just begrudgingly. Yet if there ever was a vaccination against type 1 diabetes, I would be first in line.

Researchers in France and Germany have demonstrated you can treat a type 1 diabetic mouse with a vaccination. Type 1 diabetes is an autoimmune disease in which the immune system's T cells cannot distinguish between "non-self" and "self", attacking cells of the pancreas that produce insulin.

Previously, Drs. Falk and Rotzschke of the Max Delbruck Center for Molecular Medicine (MDC), blocked the misdirected immune system by vaccinating mice with modified structures of the same organ targeted by the defective T cell immune response. Antigens are structures which activate a body's immune system, and the mice were protected from type 1 diabetes through the body's own antigens linked together in a repetive chain of identical copies. But the researchers did not understand how this protective string of antigens worked.

Chat live with Dr. Pugliese, an expert on the immunology and genetics of diabetes at The Diabetes Research Institute. His work has been focused on preventing the autoimmune attack that leads to diabetes. This research is very important for future prevention strategies, as well as stopping autoimmune destruction of transplanted islets.

Dr. Pugliese's has studied the role of the thymus gland in the immune system and he describes it as the "school for the immune system". All immune cells are forced to pass through the thymus gland where they are exposed to the antigens present throughout the body. Immune cells that bind to these normal antigens are destroyed, thereby preventing the later destruction of healthy cells. If no binding occurs, then the cell is deemed to be friendly to host tissue and is released to become part of the immune system. The insulin producing cells of the body - islets -- are not the only body cells that release insulin. Dr. Pugliese's research has shown that there are other cells that release tiny amounts of insulin, but not in response to blood glucose. These cells present insulin to the visiting immune cells in the thymus, and any immune cell that binds is killed. It is believed that a low insulin output in these decoy cells in people who develop diabetes may be the reason that immune cells are allowed to live that will later track insulin back to its source and destroy healthy islets. In people who have the genetic markers that protect against diabetes, these cells secrete more insulin than they do in people with genes that pre-dispose them to diabetes. The more insulin in the thymus, the more likely that insulin-specific autoreactive lymphocytes will be killed, with fewer chances of developing diabetes.

Confused yet? Yeah, me too - but my confusion feeds my insatiable curiosity. That is precisely why I will be joining the rescheduled chat with Dr. Pugliese. Please, be there on March 15th at 9pm Eastern Standard Time on Diabetes Talkfest. Make it a date: you, me, Dr. P and the most informed people in the diabetes community. Once again, thanks to Gina and Jon for Linking Diabetics Coast to Coast!

The Juvenile Diabetes Research Foundation announced that they have formed a partnership with MacroGenics. JDRF is providing up to $2 million to fund a clinical trial of a compound called anti-CD3 that has shown promise in slowing the progression of type 1 diabetes.

Anti-CD3 is capable of reducing the autoimmune attack that destroys insulin-producing beta cells. The treatment preserves beta cell function in newly diagnosed patients, and has the potential to decrease insulin requirements, leading to better glucose regulation, and decrease the complications of diabetes. Anti-CD3 blocks the function of CD3 cells - the T cells that destroy islets. The antibodies prevent "activation" of the T cells after they have identified their target, disarming them launching the attack on islets.

Let's hope the peace talks between JDRF, MacroGenics, anti-CD3 and killer Ts result in progressive measures to make the type 1 diabetic body a peaceful place, once and for all.

The Weizmann Institute of Science has posted a description of a new breakthrough discovery by a team of its researchers. The description can be viewed on a page of the Institute's website creatively titled the Weizmann Wonder Wander -- love it!

Basically, the big news is this: researchers have known for a while that a certain protein (HSP60) can fight Type 1 diabetes, and they have been working towards developing a vaccine for Type 1 that incorporates that protein. The Weizmann team had discovered that a peptide (p277) constituting a fragment of the HSP60 protein could shut down the autoimmune response that causes Type 1 diabetes. However, until now no one knew exactly why the protein was effective. Now we know it works like this: the p277 peptide helps regulate potentially harmful T cells. The T cells then secrete anti-inflammatory substances instead of the inflammatory ones they would normally make -- ones related to autoimmune disease. What a fantastic discovery!