June 1 (UPI) — Researchers at the Jackson Laboratory in Bar Harbor, Maine, have found a way to protect beta cells from destruction, which could lead to therapies to prevent type 1 diabetes.
Beta cells in the pancreas produce insulin. In type 1 diabetes, another type of white blood cells known as B lymphocytes work to activate the autoreactive T cells, or T lymphocytes, to destroy the beta cells in the pancreas.
The damaged cells cannot carry glucose to cells causing it to build up in the blood, leading to type 1 diabetes. Without injections of insulin, type 1 diabetics can develop damage to nerves, blood vessels and organs from high blood glucose levels.
“So there has been a lot of interest in the diabetes research community: If you can target those antigen-presenting B-cells, that could be potentially a very effective disease intervention,” David Serreze, a professor at JAX Laboratories, said in a press release. “Our approach targets an appropriate population of the B cells among the white blood cells, resulting in inactivation of the cascade of autoimmunity against the insulin-producing pancreatic beta cells, and hence subsequently blocking diabetes development.”
Researchers used gene manipulation to identify a possible metabolic target to eliminate B cells that initiate the type 1 diabetes process.
B cells turn on the gene known as activation-induced cytidine deaminase, or AID, which act like molecular scissors to cut the chromosomes within the B-cell.
The team found that non-diabetic mice treated with a specific pathway inhibitor known as AID/RAD51 had significantly more B cells capable of suppressing diabetogenic T cell responses, reducing T1D development compared to control groups.
“Ultimately, this approach could potentially be applicable to any autoimmune disease that has a B-cell component,” Serreze said.
The study was published in the Journal of Immunology.
June 1, 2017