Surprising way in which Multiple sclerosis drugs works

Cells that make myelin are sensitive to adenosine triphosphate (ATP) and nitric oxide (NO), molecules that are present in high amounts in the blood and brain lesions of MS patients. Red blood cells can release NO directly, but they can also stimulate NO production in the lining of blood vessels by releasing ATP. NO can then go on to damage nerves in MS patients.

Zinc, C-peptide-which is secreted by the pancreas along with insulin-and albumin are key players in the latter process, and they can latch onto red blood cells. Because interferon beta can bind zinc, it seemed possible that the drug helped patients by sopping up this mineral, so Dana Spence and colleagues wanted to investigate further.

In lab tests, the researchers found that red blood cells from MS patients bound more zinc, C-peptide, and albumin than cells from control subjects. Treatment with interferon beta reduced this interaction in MS samples down to control levels.

Albumin boosted zinc and C-peptide binding to MS red blood cells, and this effect went away with interferon beta treatment. From these data, the researchers conclude that it's likely the drug is inhibiting albumin binding, keeping it from delivering its cargo of C-peptide and zinc to red blood cells so that NO can be made.

Ref:

Dana Spence et. al, "Interferon-β Decreases the Hypermetabolic State of Red Blood Cells from Patients with Multiple Sclerosis", ACS Chemical Neuroscience,DOI: 10.1021/acschemneuro.2c00332 ,10-Aug-2022