Patients with Duchenne muscular dystrophy (DMD) have a genetic mutation that causes incurable muscle degeneration. Research has shown that the immune system plays a complex, double-sided role in muscular dystrophy — promoting both muscle repair and muscle degradation.
In their recent article in Frontiers in Pharmacology, Jonathan H. Soslow, MD, MSCI, Sergey Ryzhov, MD, PhD, and colleagues studied blood samples from normal people and people with DMD, and found that the patients with DMD had more T cells expressing a surface protein called CD26 compared to normal patients.
Additionally, in the DMD patients, the level of CD26-expressing T cells correlated with increased muscle strength. This may be because CD26 can bind an enzyme called adenosine deaminase (ADA), which can increase the levels of inosine, an anti-inflammatory molecule, in muscle.
The researchers hypothesize that the increased CD26-expressing cells help slow down muscle degradation in DMD patients by bringing more ADA into muscles. Their work shines a light on potential new therapeutic targets for DMD patients.
This research was supported by the National Institutes of Health (grants GM106391, GM103392, HL123938, HL121045, RR024975, TR000445), the American Heart Association, the Fighting Duchenne Foundation and the Fight DMD/Jonah & Emory Discovery Grant.
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