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'Taking treatment for autoimmune disease in a new direction'

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University of Utah Health
Nature Biomedical Engineering
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Mingnan Chen
Peng Zhao

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the United States
Salt Lake City

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Log in with your Medical News Today account to create or edit your custom homepage, catch-up on your opinions notifications and set your newsletter preferences.Sign up for a free Medical News Today account to customize your medical and health news experiences.Current treatments for autoimmune conditions rely on neutralizing the immune cells that mistakenly target and attack the body's own healthy tissue.However, a major downside of existing therapies is that they end up inactivating not just the specific immune cells causing the damage, but also other immune cells that are functioning normally.This leaves the body exposed to all kinds of other diseases and infections.Now, a research team from University of Utah Health in Salt Lake City has begun to look into disabling only the particular sets of immune cells that cause trouble in autoimmune conditions, while preserving the integrity of healthy immune cells so they can continue to do their job.The new research — conducted in mouse models — focuses on programmed cell death protein (PD-1) cells. This is the first time anyone has looked at the [PD-1] cells as a target to develop therapeutics for autoimmune disease."Study author Mingnan Chen, Ph.D.In a healthy immune system, the researchers explain, two types of specialized cells — B and T lymphocytes — express PD-1, and they feature a mechanism that checks immune cells' activity to prevent them from attacking healthy cells.In people with autoimmune conditions, that mechanism becomes ineffective, and immune cells mistakenly turn against the body.The first author of the current study, Peng Zhao, Ph.D., notes that the team "wanted to target PD-1-expressing cells" with the aim to "avoid long-term immune deficiency caused by common treatments for autoimmune disease."The researchers thus set to work to design a protein molecule that would have the effect of depleting the immune system's store of PD-1-expressing cells.This new molecule, the team explains, has three main components: an anti-PD-1 antibody fragment, the Pseudomonas exotoxin, and a protein called albumin-binding domain.Each of these three components plays a specific role: The antibody fragment attaches to PD-1-expressing cells, the toxin then kills these cells, and finally, the albumin-binding domain allows the molecule to keep circulating through the body.Once they had created this molecule, the scientists tested its effectiveness in two different mouse models: first, in one simulating type 1 diabetes and then in a model of multiple sclerosis.In the case of the rodents with a simulation of type 1 diabetes, the newly developed therapy delayed the onset of the condition.

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