Multiple Sclerosis (MS) is a neurodegenerative disease characterized by destruction of the myelin sheath surrounding nerve cells, caused by the improper functioning of the body’s innate immune cells through targeted destruction of myelin producing cells. In this paper, the researchers used a mouse model for MS known as experimental autoimmune encephalomyelitis (EAE), wherein the mouse is immunized using a myelin associated protein. This immunization causes the mouse’s immune cells to attack their own myelin covered nerves and results in the progression of disease phenotypes. This paper explores the contribution of secreted factors from the Sympathetic Nervous System (SNS) such as noradrenaline (NE) and how they contribute to the modulation of the immune response against the Central Nervous System (CNS). The authors show that increased release of NE, brought about through genetic manipulation, leads to decreased symptom progression in the mouse model, as well as showing a cellular reduction in the invasion of activated immune cells into the brain and a reduction in the release of proinflammatory cytokines, which are known to worsen symptoms. The authors also identify downstream targets of NE signalling through the Adrb2 receptor and show that inhibition of this target leads to worse symptoms of EAE (MS), in the mouse model. The paper identifies an important contribution of the SNS to EAE progression and identify specific targets for possible therapeutics in the future.
By: Nate Dempsey