New Target Can Prevent Type 1 Diabetes

In type 1 diabetes, a protein called OCA-B regulates the T cell’s activity and is responsible for the destruction of insulin producing cells. Blocking this protein can help prevent type 1 diabetes.

The researchers have identified a new target to treat patients with type 1 diabetes that blocks a protein called OCA-B. This protects the mice from type 1 diabetes by decreasing the activity of immune cells which in normal condition destroys the pancreas’ insulin-producing β cells.

The research was conducted at the University of Utah School of Medicine and was published in the Journal of Experimental Medicine (JEM)

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‘In type 1 diabetes, a protein called OCA-B regulates the T cell’s activity and is responsible for the destruction of insulin producing cells. Blocking this protein can help prevent type 1 diabetes. New therapies can be developed to target this protein.’
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In type 1 diabetes, the body’s immune system mistakenly attacks the pancreatic β cells, stopping the production of insulin. It is an autoimmune disease. These patients require life-long insulin therapy to control the blood-glucose levels. Currently, there are no treatment options that can stop the immune system from targeting β cells while still preserving its ability to fight infection.

A type of white blood cells (WBCs) called T cells can recognize specific molecules known as antigens, that are produced by bacteria and viruses that invade the body. When T cells come in contact with these antigens, they turn on hundreds of gene which can help them to fight off the infection. A protein called OCA-B binds to these genes, so that they can be easily reactivated if the T cells again encounter the same antigen later.

In most of the autoimmune diseases, the T cells mistakenly recognize and respond to antigens which are produced by normal healthy cells.

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Dean Tantin, professor at the Department of pathology University of Utah School of Medicine and also a member of the Huntsman Cancer Institute said, “Repeated antigen exposure is a common property of autoimmune responses. We therefore hypothesized that targeting OCA-B would inhibit autoreactive, diabetogenic T cell responses.”

According to the study, the mice lacking OCA-B were protected from developing type 1 diabetes. Autoreactive cytotoxic T cells that can target and kill pancreatic β cells remained inactive and did not accumulate in the pancreas. Autoreactive helper T cells which recruit other immune cells to cause inflammation accumulate in the pancreas but remain non-responsive.

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By chemically modifying the surrounding chromosomal DNA by recruiting an enzyme called Jmjd1a, OCA-B regulates the activity of T cell genes. The researchers developed a small peptide in the lab that was capable of stopping the association of OCA-B with Jmjd1a which prevented the reactivation of isolated T cells.

The activity of the autoreactive T cells can be reduced in pre-diabetic mice by injecting them with the small peptide. The glucose levels were restored to normal and the pancreatic inflammation was reduced.

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Tanin said, “While the peptide is unlikely to be used in a clinical setting, it offers a proof-of-principle for OCA-B as a therapeutic target for type 1 diabetes, and can be used as a tool for the further development of therapeutics”

Source-Medindia