Health
Focusing on beta cells instead of the immune system may be the key to preventing type 1 diabetes-ScienceDaily
Studies of the causes of type 1 diabetes often focus on the autoimmune response in which the immune system destroys islet beta cells that produce insulin. A new study by scientists at the University of Chicago instead focuses on the role of beta cells themselves in inducing autoimmunity. The study also raises the possibility that new drugs will prevent the immune system from destroying beta cells and prevent type 1 diabetes from developing in at-risk and early-onset patients.
Research published today Cell reportExplains how researchers can use gene tools to knock out or remove genes called Alox15 Mice with a genetic predisposition to develop type 1 diabetes. This gene produces an enzyme called 12 / 15-lipoxygenase. It is known to be involved in the process that causes inflammation in beta cells.delete Alox15 In these mice, we maintained beta cell levels, reduced the number of immune T cells infiltrating the islet environment, and prevented the development of type 1 diabetes in both men and women. These mice also showed increased expression of a gene encoding a protein called PD-L1, which suppresses autoimmunity.
“The immune system does more than just decide to attack the beta cells one day. In our opinion, the beta cells themselves are somehow radically altered to induce their immunity,” said the senior. Author Raghavendra Mirmira, MD, PhD, Professor said. She is the director of the School of Medicine and the Center for Diabetes Translation Studies at UChicago.
“When we removed this gene, beta cells no longer signaled the immune system, and even without touching the immune system, the immune onslaught was completely suppressed,” he said. “It tells us that there is a complex dialogue between beta cells and immune cells that can be intervened to prevent diabetes.”
This study is the result of a long-term collaborative study that began when Milmira and several members of his lab were at Indiana University. Dr. Jerry Nadler, Dean of Medicine and Professor of Medical Pharmacology at New York Medical College, discovered the role of the 12 / 15-lipoxygenase enzyme, and Dr. Maureen Gannon is a professor of medicine, cell and developmental biology, Vanderbilt. The University’s Molecular Physiology and Biophysics provided the strains of mice used in the study. This will result in Alox15 The gene when a drug called tamoxifen was administered.
In 2012, Dr. Sarah Tarcy, an assistant research professor at the University of Chicago and co-lead author of the new study, led a project that first suggested that beta cells may play a central role in the development of type 1 diabetes. Did.
“This gives us an understanding of the underlying mechanisms that lead to the development of type 1 diabetes,” says Tersey. “This is a major change in the field, focusing on the role of beta cells, not just autoimmunity.”
This study also has interesting implications for cancer treatments that utilize the immune system to fight tumors. Cancer cells often express the PD-L1 protein, which suppresses the immune system and evades the body’s defenses. New drugs, called checkpoint inhibitors, target this protein, blocking or eliminating the “checkpoints” of PD-L1 and releasing the immune system to attack tumors. In a new study, increased PD-L1 in knockout mice serves its intended purpose by preventing the immune system from attacking beta cells.
In a new study, researchers also tested drugs that block the 12 / 15-lipoxygenase enzyme on human beta cells. They confirmed that this drug, called ML355, increased PD-L1 levels. This suggests that it may interfere with the autoimmune response and prevent the development of diabetes. Ideally, it should be given to patients who are at high risk due to their family history and who show early signs of developing type 1 diabetes, or immediately after diagnosis and before excessive pancreatic damage occurs. Milmira and his team have taken the first step in initiating clinical trials to test possible treatments with the ML355.
“This study does suggest that inhibition of the enzyme in humans can increase PD-L1 levels, which is very promising,” says Mirmira. “Beta cell-targeted therapies can catch an individual before the process begins and completely prevent the disease from progressing, unless the disease has progressed until the beta cells are destroyed in large numbers.” believe.”
Story source:
material Provided by University of Chicago.. Original written by Mattwood. Note: Content can be edited in style and length.
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Sources 2/ https://www.sciencedaily.com/releases/2022/06/220628113322.htm The mention sources can contact us to remove/changing this article |
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