- The specific pathways that lead to the development of type 1 diabetes remain a mystery.
- Some researchers have focused on the role of chemokine ligand 2, an inflammatory cytokine (CCL-2).
- The specific nature of the link between CCL-2 and type 1 diabetes, however, remains unknown.
- A new study adds to the picture and may open up new possibilities for treating or delaying the onset of type 1 diabetes.
According to the American Diabetes Association, type 1 diabetes affects roughly 1.6 million people in the United States.
Diabetes type 1 is an autoimmune illness. It occurs when the pancreas’ immune system attacks and destroys beta cells. The insulin-producing beta cells are grouped together in islets.
Although scientists have known for some time that type 1 diabetes is an autoimmune disease, it is still unknown why the immune system should activate the pancreas.
Some researchers are seeking for signs in the interaction between genes and the immune system as study progresses.
A new study published in the Journal of Translational Autoimmunity looks into the involvement of a specific gene in the development of type 1 diabetes.
Scientists have already linked type 1 diabetes to a certain chromosomal segment. However, they were baffled as to why this region, known as locus 3p21.31, affects risk. The current research adds to the picture.
This area of the genome codes for a variety of proteins, including the CCR2 receptor. CCR2 activates T lymphocytes and recruits macrophages when it binds to the cytokine CCL-2, causing inflammation.
While scientists have previously investigated the link between CCL-2 and type 1 diabetes, the findings have proven challenging to interpret.
According to researchers, CCL-2 levels differ between those with type 1 diabetes and those who do not have the disease. However, some studies have discovered higher amounts, while others have discovered lower levels.
CCL-2: A fresh perspective
The researchers used data from the Diabetes Autoimmunity Study in the Young to study this perplexing association. Daisy began tracking 310 newborns at high risk of developing type 1 diabetes from birth in 1993.
42 of them acquired islet autoantibodies but didn’t develop type 1 diabetes. To put it another way, their immune systems had responded to insulin-producing cells in the pancreas but had not yet progressed to type 1 diabetes. The writers refer to this group as nonprogressors.
The authors refer to this group as the “progressors” because 48 of the participants developed type 1 diabetes. The patients were compared to a control group of 220 adults who did not have islet antibodies or type 1 diabetes.
When compared to controls, blood levels of the cytokine CCL-2 were considerably lower in both progressors and nonprogressors. The authors noticed a gradual reduction in CCL-2 levels as autoantibody-positive individuals proceeded to type 1 diabetes.
They also discovered that these two groups had higher levels of CCR2, a receptor that binds CCL-2 on immune cells.
According to the authors, more CCL-2 binds to receptors when there are more receptors available. It attaches to the pancreas, causing inflammation and damage. Furthermore, because CCL-2 is attached to a receptor, free-floating CCL-2 levels in the blood decrease.
The authors conclude that decreasing CCR2 may help people with islet autoantibodies avoid developing type 1 diabetes. They express themselves as follows:
“Inhibition of CCR2 could slow the recruitment of immune cells to the pancreatic islet, such as T cells and monocytes, and hence postpone the onset of islet autoimmunity.”
The genetics of type 1 diabetes
The importance of studying the function of genes in type 1 diabetes was discussed with MNT by Dr. Faye Riley, senior research communications officer at Diabetes UK. She stated, “
“Scientists are working on type 1 diabetes risk calculators that utilize genetic information to identify youngsters who are more likely to develop the disease later in life.”
“Right now, risk scores are being used to identify persons who might benefit from participating in a clinical study of immunotherapy to delay or prevent type 1 diabetes.” Genetic risk calculators could potentially be used as a screening tool to identify children who will benefit from the treatment in the future, once immunotherapies are allowed for use outside of a research context.”
“Identifying which genes are linked to type 1 diabetes gives us a way to spot those at higher risk of developing the condition,” Dr. Riley told MNT.
“Knowing more about the genetics of type 1 diabetes could help us better understand what causes the disease, potentially leading to new prevention and treatment techniques,” Dr. Riley added.
Despite the fact that the research was conducted on a small group of participants, the findings appear to suggest that inhibiting CCL-2 may lessen the risk of getting type 1 diabetes. Of course, further research is required before this method can be used in the clinic.
