PHILADELPHIA,
July 31,
2024 /PRNewswire/ -- Mast cells are found throughout
the body close to blood vessels and are packed with granules
containing the immune signaling compound histamine, and enzymes
that attack pathogens and promote white blood cell recruitment.
When triggered by a perceived threat, mast cells expel their
contents. This activity protects against infection and aids
healing, but it has also made mast cells infamous for driving
allergic asthma and inflammatory skin disorders, such
as rosacea and contact dermatitis.
Despite their prominence, few researchers study
these scarce and difficult-to-work-with cells. Hydar Ali, a
professor in the Department of Translational Sciences at Penn
Dental Medicine, belongs to a select group who focus on mast cells.
His research explores how they function to protect the body and how
things can go wrong.
"These cells are relatively poorly understood,
and yet we've been able to identify some of the most sought-after
molecular targets to affect diseases like allergies and asthma that
have the potential to kill," Ali says.
He and his colleagues discovered a receptor,
known as MRGPRX2, that only appears on mast cells. This research
led them to find that small proteins called antimicrobial peptides
could activate mast cells through MRGPRX2 to harness their
protective function and help clear pathogens. In the context of an
allergic response, however, he has shown that this receptor drives
problematic inflammation.
"It's two sides of the same coin," Ali says.
More recently, his team has investigated mast
cells' role in systemic allergic reactions that can lead patients
to stop using the multiple sclerosis drug glatiramer acetate. Their
experiments demonstrated that this medication activates MRGPRX2
receptors causing mast cells to expel histamine and their other
contents, results suggesting MRGPRX2 inhibitors could treat these
reactions and help patients remain on the medication.
His lab is also investigating this receptor's
role in periodontal disease, an inflammatory condition that damages
the gums and connective tissue of the mouth. Their experiments have
shown, for example, that mast cells expressing MRGPRX2 become more
abundant in chronic periodontitis, the more severe form of the
condition. Ultimately, he hopes to study the potential for MRGPRX2
blockers to reduce inflammation in periodontitis.
Media Contact: Beth Adams,
adamsnb@dental.upenn.edu
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SOURCE PENN DENTAL MEDICINE