TYPE 1 DIABETES RESEARCH - ADVANCES TYPE 2 DIABETES & AUTOIMMUNE DISEASES RESEARCH EFFORTS
Because of the multifaceted nature of the disease, type 1 diabetes has much in common with other conditions, including type 2 diabetes and its complications as well as autoimmune diseases such as psoriasis, rheumatoid arthritis, celiac disease, and lupus. Finding common ground between type 1 diabetes research and other fields will accelerate the search for cures that extend well beyond the type 1 diabetes population. JDRF supports a vigorous and sustained research effort to cure type 1 diabetes that may translate into novel therapies and lead to solutions for many diseases.

TYPE 1 DIABETES RESEARCH – BENEFITS PEOPLE WITH TYPE 2 DIABETES
Type 1 diabetes and the most prevalent form of the disease--type 2 diabetes--begin in very different ways. In type 1 diabetes, a complex interplay of genetic and environmental factors triggers an autoimmune process in which a person's immune system mistakenly attacks and destroys normal insulin-producing tissue in the pancreas. Type 2 diabetes is also influenced by genetic and environmental factors but, unlike in type 1 diabetes, diet and lack of exercise are among the primary triggers. Rather than a lack of insulin, type 2 diabetes patients produce extra insulin in the early stages of the disease, although cells throughout the body are "resistant" to insulin action.

Researchers are finding that despite the different causes of type 1 and type 2 diabetes the long-term consequences are remarkably similar. Both forms of diabetes are characterized by abnormally high levels of glucose in the blood, which gradually damages blood vessels and nerves throughout the body. This damage can lead over time to blindness, kidney failure, non-healing ulcers, heart disease, and other serious complications. Researchers have shown that the underlying mechanisms of complications are nearly identical between the two diseases, giving hope that new therapies developed for one population will be effective in the other. For example, two major clinical trials--the Diabetes Control and Complications Trial (DCCT) of type 1 diabetes patients and the UK Prospective Diabetes Study (UKPDS) of type 2 diabetes patients--came to the same conclusion: better glucose control could dramatically reduce the risk of long-term complications.

A vigorous research effort to replace or restore beta cell function will benefit patients with either form of diabetes. For example, islet transplantation has been proven in type 1 diabetes patients to restore insulin production, reverse symptoms of hypoglycemia unawareness, and stabilize or halt the progression of some long-term complications. As new research continues to optimize islet transplantation, including the development of less toxic immune suppression drugs, this procedure may be extended to benefit type 2 diabetes patients. Similarly, individuals with either disease will one day be helped by research to regenerate beta cells within the pancreas without the need for transplantation. In the short term, research on an artificial pancreas that automatically links glucose measurement and insulin delivery will greatly improve the daily burden of disease management for type 1 diabetes patients as well as type 2 diabetes patients who have become insulin-dependent.

TYPE 1 DIABETES RESEARCH – BENEFITS PEOPLE WITH OTHER AUTOIMMUNE DISEASES
Autoimmune diseases result when the immune system that normally protects the body from foreign invaders such as bacteria or viruses goes awry and attacks healthy tissue. In type 1 diabetes, the autoimmune attack destroys the pancreatic beta cells. In other diseases, the immune system may damage the skin (psoriasis), joints (rheumatoid arthritis), intestinal lining (celiac disease), connective tissue (lupus), or other organs. Overall, the Autoimmune Diseases Coordinating Committee of the NIH counts more than 80 autoimmune diseases that collectively affect as many as 23.5 million Americans.

Autoimmune disorders have a complex pattern of inheritance, where multiple genes interact with environmental factors to produce a disease. Nevertheless, it is clear that there are overlapping regions of genetic susceptibility as well as common underlying immune mechanisms. At least one of the genetic factors involved in the development of most (if not all) autoimmune diseases is located in the major histocompatibility complex (MHC), the genetic region containing the genes that are responsible for recognition of self and non-self. Data from animal models of autoimmunity also suggest a potential sharing or overlap between non-MHC genes associated with susceptibility to type 1 diabetes, systemic lupus erythematosus, and multiple sclerosis. Other genes known to determine susceptibility to type 1 diabetes, such as CTLA-4 and PTPN-22, are also involved in other autoimmune diseases.

Possible environmental triggers such as viral infection or vitamin D deficiency are thought to play a role in the onset of autoimmune diseases in genetically at-risk individuals. Due to the common origins of autoimmunity, development of drugs to combat one disease may have far-reaching benefits for many autoimmune disease patients. For example, the anti-CD3 drug originally developed for use in kidney transplantation had significant side effects that limited its clinical usefulness, particularly in children. Development of a less-toxic, modified version of anti-CD3 was then tested in newly diagnosed type 1 diabetes patients, including some as young as 7.5 years old. Clinical trials showed that this drug could modulate the immune system and alter the clinical course of new onset type 1 diabetes. The improved safety profile of modified anti-CD3--first tested in diabetes has led researchers to launch additional trials in ulcerative colitis, Crohn's disease, and psoriasis, among other diseases.