The team were able to show that P2X7R is expressed in peripheral monocytes of MS patients and that its channel function is intact. Importantly the channel response was more pronounced in MS patients versus healthy control monocytes. Steroids are generally used to treat MS relapse and their mechanism of action is not entirely clear. We were able to show that dexamethasone can induce monocyte cell death. Also
examining some of the downstream mediators of P2X7R function, we were able to show that MS patient monocytes were capable of releasing a higher level of the proinflammatory cytokine, IL-1β. These results are highly relevant in the field of MS relapse and MS relapse related neuroinflammation.
