About 400,00 individuals are affected by multiple sclerosis (MS) in the United States and about 2.3 million people worldwide (National Multiple Sclerosis Society, 2002). The majority of symptoms commence between ages 20 and 40, with greater risk for women to be twice as likely to develop the disease (National Institute of Health, 2014). The exact cause of MS is unknown but there research shows there are geographic (people who live further from the equator), genetic, race (Northern European descent), smoking, and infectious agents (such as Epstein-Barr virus) know to be associated with the disease (Mayo Clinic, 2014). With my experience working in a neurology unit, I have seen a significant number of patients who are affected by this disease.
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In MS, there is demyelination (loss of myelin sheaths) in the central nervous system (CNS), leading to scarring and/or plaque formation and ultimately resulting in the loss of axons. Autoreactive B and T cells attack myelin autoantigens and cause inflammation in white matter in the CNS (McCance & Huether, 2014). B cells produce autoantibodies, secrete inflammatory cytokines, activate complement, and activate T cells by presenting the antigen. Activated CD4+ and CD8+ T cells cross the blood brain barrier, enter the CNS and attack myelin (McCance & Huether, 2014). Pro-inflammatory cytokines interleukin-12 (IL-12), IL-23, IL17 and lack of IL-10, an anti-inflammatory cytokine all contribute to exacerbation of the inflammatory process (McCance & Huether, 2014). Integrin expression facilitates adherence and passage of immune cells into the CNS. B lymphocytes and plasma cells contribute to the inflammation and damage to the myelin and axons. B cells are more active in chronic or progressive types of MS (McCance & Huether,
In MS, there is demyelination (loss of myelin sheaths) in the central nervous system (CNS), leading to scarring and/or plaque formation and ultimately resulting in the loss of axons. Autoreactive B and T cells attack myelin autoantigens and cause inflammation in white matter in the CNS (McCance & Huether, 2014). B cells produce autoantibodies, secrete inflammatory cytokines, activate complement, and activate T cells by presenting the antigen. Activated CD4+ and CD8+ T cells cross the blood brain barrier, enter the CNS and attack myelin (McCance & Huether, 2014). Pro-inflammatory cytokines interleukin-12 (IL-12), IL-23, IL17 and lack of IL-10, an anti-inflammatory cytokine all contribute to exacerbation of the inflammatory process (McCance & Huether, 2014). Integrin expression facilitates adherence and passage of immune cells into the CNS. B lymphocytes and plasma cells contribute to the inflammation and damage to the myelin and axons. B cells are more active in chronic or progressive types of MS (McCance & Huether,