What is the mechanism of action for monoclonal antibodies used in MS therapies?

Monoclonal antibodies used in multiple sclerosis (MS) therapies primarily function by targeting specific immune cells to reduce inflammation. MS is an autoimmune disorder where the immune system mistakenly attacks the central nervous system, causing inflammation and damage to the myelin sheath that protects nerve fibers.

Monoclonal antibodies are designed to selectively bind to certain proteins or cells involved in the immune response. By targeting specific immune cells, such as B cells or T cells, these therapies reduce the activity or proliferation of these cells, thereby decreasing the inflammatory processes that contribute to MS progression and symptoms. This targeted approach helps to mitigate the inflammatory attacks on the nervous system, leading to potential stabilization or improvement in clinical outcomes for patients with MS.

Other options do not appropriately reflect the specific mechanism of action of these therapies. For instance, blocking all neurotransmitters would lead to a generalized disruption of neural activity, which is not the objective in MS treatment. Enhancing muscle contractions does not address the underlying immune-mediated pathology. Similarly, inhibiting nerve signal transmission would be counterproductive in managing a disease where preservation of nerve function is crucial. Thus, focus on targeted immune modulation represents a more effective strategy in treating MS.