Abstract
Multiple sclerosis (MS) is an autoimmune disorder in cause the demyelination of neurons, resulting in degenerative symptoms. MS activates inert autoreactive myelin T‐cells, lymphocytes specific to the destruction of central nervous system myelin, to cross the blood brain barrier and secrete inflammatory cytokines, recruiting other leukocytes and macrophages that demyelinate axons primarily through the release of myelinotoxic substances. The most effective treatment for MS is administration of β interferon, which reduces relapse rate of nervous tissue attacks. The Marshfield SMART Team (Students Modeling A Research Topic) designed a model of β interferon using 3D printing technology to understand its interaction with T‐cells to treat MS. β interferon is an endogenous polypeptide that regulates T‐cells and are hypothesized to convert autoreactive myelin T‐cells into suppressor cells that can deactivate other myelin targeting lymphocytes. β interferon may also lead to the inhibition of cytokines, preventing activation of the autoreactive T cells. Interferons may inhibit the leukocyte migration across the blood‐brain barrier to prevent access to myelin. Understanding the structure and function of β interferon could lead to more precise and effective drugs to treat MS. Supported by grants from the Marshfield Clinic Research Foundation and NIH‐SEPA.
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