Exogenous activation of tumor necrosis factor receptor 2 promotes recovery from sensory and motor disease in a model of multiple sclerosis

This study explores the therapeutic potential of activating tumor necrosis factor receptor 2 (TNFR2) in a mouse model of multiple sclerosis (MS). The researchers found that systemic administration of a TNFR2 agonist alleviated both peripheral and central inflammation. The treatment reduced demyelination and neurodegeneration, suggesting that the protective signals induced by TNFR2 outweigh any potential harmful effects. Behavioral data indicated that a TNFR2 agonist is therapeutic on motor symptoms and promotes long-term recovery from neuropathic pain. The study suggests that activating TNFR2 could be a promising therapeutic approach for treating motor and sensory diseases in MS, as well as other inflammatory diseases or neuropathic pain conditions, due to its dual mode of action in suppressing CNS autoimmunity and promoting remyelination.

• 1
  Systemic administration of a TNFR2 agonist alleviates sensory and motor deficits in EAE, indicating that protective responses via Tregs and/or CNS-resident cells exceed potential pathogenic responses.
• 2
  TNFR2 agonist administration expands peripheral Treg levels but does not impact macrophage activation, suggesting an immunosuppressive effect without interfering with macrophage activity.
• 3
  TNFR2 agonist administration reduces neurodegeneration and demyelination in the spinal cord, indicating a protective effect on nerve cells and myelin.