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autoimmune diseases, such as type 1 diabetes and multiple sclerosis, the body's
immune system mistakenly attacks healthy cells, believing them to be harmful
agents. Recently, scientists have been conducting new research with the aim of
devising an innovative strategy to treat these conditions.
Recent research explores a promising
new pathway in the treatment of autoimmune conditions.
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. PD-1 is a type of protein on the surface of certain
cells, and it plays a key role in regulating the immune response.
The
study's findings, which were published yesterday in the journal Nature Biomedical Engineering,
suggest that the new strategy may be a viable, more constructive approach to
tackling autoimmune conditions.
"We are really taking treatment for autoimmune disease
in a new direction. 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.
3 key components working in unison
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.
Novel approach 'could make a huge impact'
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. Usually, diabetes-like
symptoms would set in at 19 weeks in mice, but those that had received the new
treatment only began developing such symptoms at 29 weeks.
Then, when the researchers tested the new molecule
in a mouse model of multiple sclerosis, they saw even more encouraging results:
The treatment stopped paralysis progression in the six mice involved. Moreover,
these rodents even regained the ability to walk.
The
researchers continued to monitor these mice for 25 days following treatment and
found that the therapy continued to keep paralysis at bay.
While
the scientists are very enthusiastic about how promising this new approach
appears to be, they nevertheless caution that the molecule they developed can
so far only be applied to mice.
"To
make similar therapeutics for people, we would need to find the anti-human PD-1
antibody, like the anti-mouse PD-1 antibody," explains Chen. Still, he
expresses hope that this is an achievable goal that may improve the outcomes
for people living with autoimmune conditions.
"If we can generate the human version of
therapeutics, I think we could make a huge impact in treating autoimmune
disease," Chen says.
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