Abstract:

Bone Morphogenetic Proteins (BMP) and Transforming Growth Factor-beta (TGF-β) are cytokines with similar receptors and messengers. They are important for immune cell function, with BMPs exerting mainly proinflammatory but also anti-inflammatory effects, and TGF-β suppressing inflammation. Patients with Multiple Sclerosis exhibit BMP overactivity and suppressed TGF-β signaling. This dysregulated signaling participates in the crosstalk between infiltrating immune cells and glia, where BMP inhibits remyelination. Reciprocal antagonism between the two pathways takes place via a variety of mechanisms. Although this antagonism has not been studied in the setting of Multiple Sclerosis, it could inform further research and treatment discovery.