Scientists identify immune system regulator that may delay onset of type 1 diabetes
Discoveries have enabled scientists to discover a regulatory factor in the immune system that may delay the onset of type 1 diabetes giving hope to thousands of people around the world with diabetes.
Calorie-restricted diets can give some people type 1 diabetes many others type 2 diabetes and the need for rule-1 diabetes known as autoimmune type 1. Type 1 diabetes is associated with shrinking of blood supply to the pancreas and alters insulin-producing cells and the blood sugar.
Gold-standard techniques for exploring how the immune system can affect the brain in the early stages of development into adulthood-;which includes using the blood of healthy people or mice to model immune cell activity inside individuals experiments using such animals or mice that can develop type 1 diabetes-;are not easily available said Dr. Joshua Tan a postdoctoral fellow at Yale School of Medicine (YSM) in New Haven Connecticut and co-leader of the team that discovered the factor.
In the study published by Nature Immunology Tans team reported a connection between type 1 diabetes and an immune system protein called Th17 helper T (Th9) which was overexpressed in type 1 diabetes finding the protein to be a central link in the chain of causation. This maintained a relationship between the two disorders and added important new research into the immune system as a potential target of prevention and treatment for both diabetes and eczema.
There are a number of interventions that are known to reduce the risk or probability of developing type 1 diabetes because these help to fix the progression of these diseases. Our study lays the foundation for such a paradigm shift in way we think about the immune system functioning in the same populations and is an important milestone in developing new insights into this devastating disease said Tan a clinical instructor in the Novo Nordisk Foundation Center for Basic Metabolic Research at YSM.
The thrombocytopenia protein (TTP) – a protein that has been overexpressed in several autoimmune diseases since the 1970s – shows up both in healthy and diabetic mouse blood and human peripheral (skin) tissue. TTPs presence in the blood of healthy people is a prerequisite for the onset of type 1 diabetes and while the molecular mechanisms of how TTP contributes to allergicdiabetic autoimmune symptoms are not well understood.
More than 360 million people worldwide are affected by type 1 diabetes which are most common in developing countries. Approximately 50 to 61 million of the current victims are children and teens. In the U. S. 2. 1 million adults and 2. 5 million children are estimated to be estimated to carry the autoimmune form of disease. About 67 million people worldwide are estimated to be affected by common autoimmune disorders including red red skin psoriasis rheumatoid arthritis and lupus.
The Th17 helper T regulatory factor (Th9) is widely found in the immune system making it one of the classical immune regulatory factors for TTP. Analysis of Th9 expression in cystic fibrosis and other fibromyalgia associated autoimmune encephalopathies showed a few sites in the Th17 regulatory subfamily had specific expression suggesting it may be important for modulation of TTP. Acquired Th17 immune activation has been previously reported in hypoxic conditions such as hypoxic mycobacterial skin infection and it was known to contribute to autoimmune-related skin symptoms to a subset of patients with systemic lupus erythematosus.