Multiple sclerosis (MS) is an autoimmune disease that causes damage to the tissue of central nervous system (CNS). Specifically, multiple sclerosis results from unregulated inflammation that damages a nerve’s myelin sheath – protective coating that protects and insulates the axon of a nerve cells. When the myelin is damaged, transmission of CNS signals is slow and inefficient [1]. Damaging inflammation can occur in the brain, optic nerve, and spine and result in a variety of debilitating symptoms including: muscle spasms, numbness, tremors, weakness, difficulty walking, and problems with coordination [2].
Previous research has confirmed that CD8 T cells significantly contribute to the pathogenesis, or development of multiple sclerosis. Activated CD8 T cells are believed to secrete pro-inflammatory cytokines, or intracellular chemical signals, which release lytic enzymes upon recognition of a target cell surface receptor. Lytic enzymes are proteins that facilitate the breakdown of cell components. CD8 T cells bind to target cells that are damaged or infected with a pathogen, and release a granule containing lytic enzymes. The binding of an activated CD8 target cell initiates granule mediated cell destruction. In the case of MS, autoreactive CD8 T cells bind to healthy nerve cells and release lytic enzymes, resulting in damage to the myelin sheath [3].
Schneider and colleagues argue that IL-15 significantly contributes to the development of multiple sclerosis. IL-15 is a cytokine that regulates the development, activation, and proliferation of CD8 T cells. Previous research has concluded that elevated levels of IL-15 have been detected in a number of inflammatory diseases including rheumatoid arthritis, celiac disease, psoriasis, and inflammatory bowl disease. Additionally, elevated levels of IL-15 have also been identified in the peripheral blood of MS patients. In the present study, researchers hope to explore the role that B cells play in producing IL-15 in the peripheral blood of MS patients. In addition, the authors hope to explore the effect of IL-15 on enhancing CD8 T cell activity.
