Auto immune disorders arise when the body starts producing an inappropriate immune response against its own cells and tissues. This happens when the immune system fails to recognize one or a number of its body constituents and starts producing auto antibodies which end up attacking its own cells, tissues and organs. This results to inflammation and damage leading to auto immune disorder. Some of auto immune disorders can be triggered by a bacteria or virus but they are very few. This happens when antibodies or T cells attack normal body cells since they have some structures which are like for the infection microorganism.
These disorders are categorized into two i. e. systemic and localized auto immune disorder. Multiple Sclerosis lies under the class of localized auto immune disorder ( http://www. themcfox. com/multiple-sclerosis/ms-drugs/rebif/rebif-autoimmune. htm as retrieved on 5 Mar 2008 00:59:29 GMT). Multiple sclerosis has significant immunological aspects and its treatment is immunomodulatory. The disease is an auto immune disorder which portrays some symptoms such as demyelinization, inflammation and axonal and also neuronal loss. Its diagnosis is extensive since it has multiple anatomical sites.
Clinical diagnosis is done by knowing the history and physical features of the disease so as to determine the multiple anatomical sites which the disease has invaded. Multiple sclerosis is a chronic disorder of central nervous system and impairment and disability increases over the period of time. The four clinical features of multiple sclerosis are:- – Relapse of multiple sclerosis- This occurs when there is complete or incomplete recovery as a result of acute exacerbation and disability occurs which is viewed as secondary progressive multiple sclerosis.
– Secondary progressive multiple sclerosis- This is mainly the cause of neurological disability in young adults. – Progressive multiple sclerosis. – Progressive multiple sclerosis. Multiple sclerosis has sub-clinical period whereby minimum or no clinical features are seen and MRO activity may occur which are picked up incidentally. Demyelinating plague may occur with hyperitensity on T1. Immunological aspect of multiple sclerosis is quite complex. An over view of it shows that there are some foreign particles or molecules at the periphery, some proteins and antigens which appears and mostly they originated from viral insult.
The molecule is then engulfed by an antigen preventing cell (APC) (Sudhir, 1999). Engulfment by APC is usually a macrophage or it can involve other peripheral cells in the blood and they usually have external grooves which posses the antigens. When foreign molecules combine with APC, they determine major histocompactibility of the complex (MCH). Then MCH is usually noted by the T. cells which activate power can be increased by CD40. CD 40 undergoes clonal expansion and then it undergoes differentiation in TH1 and TH2 cell receptors. TH1 acts as pro-inflammatory T cell whereas the TH2 acts as ant-inflammatory T cell.
In multiple sclerosis (MS) mainly there is cytokine imbalance. A normal individual has balance between the inflammatory and anti inflammatory which is TH1 cell and in this case the anti inflammatory cells are always reduced. In MS inflammatory markers (IFN y) are IL12 and tumor necrotic factors (TNF) while anti inflammatory markers are, IL4, IL10, and PGF Beta. Therefore when individuals with MS are being treated, the target is to maintain balance between the TH1 and TH2 cell or to make the T cell to shift to an anti inflammatory bias which will result to more TH2 cells.