Show simple item record

dc.contributor.authorBalestrino, Matthew
dc.date.accessioned2009-01-14T16:59:17Z
dc.date.available2009-01-14T16:59:17Z
dc.date.issued2009-01-14T16:59:17Z
dc.identifier.urihttps://hdl.handle.net/1813/11726
dc.description.abstractMultiple 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.en_US
dc.language.isoen_USen_US
dc.subjectmultipleen_US
dc.subjectsclerosisen_US
dc.subjectsimulationen_US
dc.subjectcytokineen_US
dc.titleCytokine Imbalances in Multiple Sclerosis: A Computer Simulationen_US
dc.typedissertation or thesisen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

Statistics