cytokine imbalances in multiple sclerosis a computer.docVIP

Cytokine Imbalances in Multiple Sclerosis: A Computer Simulation Matt Balestrino Abstract Multiple sclerosis is a T cell autoimmune disease that results in the formation of inflammatory lesions and breakdown of the blood-brain barrier. Little is known about the mechanisms by which lesions form and propagate, but researchers speculate that TH-17 CD4+ T cells, characterized by interleukin-17 (IL-17) production, play a critical role in disease progression. Interleukin-23 (IL-23) is primarily responsible for the activation of TH-17 T cells. IL-23 production by dendritic cells is increased in patients with multiple sclerosis, but the reasons why are not known. A computer model was developed to test the feasibility of a point mutation in PTPRC as the cause for increased production. Results show that it is possible for a point mutation to cause a ten-fold increase in IL-23 concentration over five years. Increases in IL-23 concentration lead to increased levels of IL-17, which may make considerable contributions to the severity of the disease. More research needs to be performed on the effects of IL-17 on the various cells of the immune system. Introduction Multiple sclerosis (MS) is an autoimmune disease characterized by the formations of acute inflammatory lesions and the breakdown of the blood-brain barrier (BBB). Little is known about its onset and the mechanisms involved in myelin degradation1. Many researchers argue genetic disposition for contraction combined with environmental factors, however genetic factors are largely unknown1. Case studies by Jacobsen et al demonstrated an association between a point mutation in the gene (PTPRC) encoding protein-tyrosine phosphatase, receptor-type C (CD45) and the development of MS2. Considerable research has also been dedicated to finding a specific antigen involved in MS3. Because of its similarities to experimental allergic encephalomyelitis (EAE) in mice, the focus of this research has been on myelin proteins, bu