Duke University Medical Center
research The Garcia-Blanco Lab

Stephanie Arvai
Research Analyst

Stephanie Arvai Elon University
BS, Sports Medicine: Exercise Sports



  Phone: 919.681.2658
Email: stephanie.arvai@duke.edu 

Research Interests

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the fatty substance called myelin that surrounds the nerves in the brain and the spinal cord. Myelin insulates the nerves and enables them to conduct impulses between the brain and other parts of the body. The damage to the myelin that occurs in MS impairs the ability of nerves to transmit their signals, leading to a wide range of physical and cognitive issues that vary greatly from patient to patient. Symptoms may be mild, such as numbness in the limbs, or severe, such as paralysis or loss of vision. Unfortunately, the exact cause of MS is still unknown.

Animal models of human disease are often used in research to allow scientists to gather information about a disease without harming a human in the process. Currently the most commonly used animal model of MS involves the induction of CNS inflammation in young adult mice with myelin antigens (such as MBP, PLP, and MOG) and pertussis toxin which will break down the blood brain barrier, this animal model is known as Experimental Autoimmune Encephalomyelitis (EAE). However, this method has downfalls including lack of spontaneous disease development, B Cell involvement, and lack of a genetic aspect. With this imprecise model and the recent discovery of the involvement of the alternatively spliced soluble form of the Interleukin-7 receptor we have decided to create a new transgenic (Tg) mouse model that will produce the soluble receptor found in humans that has been linked to MS. It is our hope that this Tg mouse will spontaneously develop a chronic and remitting form of MS that will more closely resemble the human disease course and which will allow us to study in vivo the effects of the soluble form of Il-7 and its role in MS.


Racioppi L, Noeldner PK, Lin F, Arvai S, Means AR. 2012. Calcium/calmodulin-dependent protein kinase kinase 2 regulates macrophage-mediated inflammatory responses. J Biol Chem. 287(14):11579-91.