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In type 1 diabetes, the body's immune system mistakenly attacks the pancreatic beta cells that produce insulin
Can the immune system's attack on islet B cells slow down? A research team from Linköping University, Sweden, recently published a phase 2b trial in Diabetes Care, a journal of the American Diabetes Association (ADA).
In type 1 diabetes, the immune system usually forms antibodies against a protein called GAD65 (glutamate decarboxylase)
This study aims to vaccinate GAD components for patients with elevated GAD antibodies, hoping to make the immune system more tolerant of the body's own GAD, thereby stopping the destruction of pancreatic β cells and promoting insulin secretion
The researchers recruited a total of 109 recipients between the ages of 12 and 24 who were diagnosed with type 1 diabetes in the near future (7 days to 193 days), elevated serum GAD65 autoantibodies, and fasting serum C-peptide >0.
In the experimental group, the researchers injected 4 μg of GAD (one injection per month, 3 times in total) and oral vitamin D (2000 IE per day for 120 days); while the control group received a placebo
The research team also focused on the subgroup of patients carrying the HLA DR3-DQ2 gene
A gene called HLA DR3-DQ2 exposes the GAD protein (GAD65) on the surface of β cells to the immune system, triggering the immune system to produce antibodies against the protein and destroying β cells
It was found that although the treatment group and the placebo group had no difference in the degree of maintaining insulin production
During the study, no adverse reactions that may be related to GAD injection were observed
The researchers pointed out in the paper that injecting GAD protein into the human lymphatic vessels is a simple and well-tolerated treatment for type 1 diabetes; at the same time, vitamin D supplementation seems to retain the newly developed type 1 diabetes patients carrying the HLA DR3-DQ2 gene.
Reference materials:
[1] Ludvigsson, J.
[2] Diabetes vaccine gives promising results in a genetic subgroup.