Rheumatoid Arthritis: The Cause Of Autoimmune Disease

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There are many autoimmune diseases that affects a 5% of the population. This occurs when the immune system can not detect the difference between self and nonself. The human immune system protects the body from foreign virus’ and sends antibodies to kill the unknown virus. This disease then causes the body to produce antibodies that will attack against the body’s healthy cells. It proceeds to attack itself and it’s healthy body cells. The actual cause of autoimmune disease is unknown. One theory is that patients are more disposed to the autoimmune disease through genes and their genetic makeup.
Rheumatoid arthritis is a chronic and one of the most common autoimmune diseases that affect 0.5% - 2% of the population, especially in females. This
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A deficiency in the female hormone, estrogen, will decrease bone restoration which could eventually lead to greater possibility of osteoporosis. This female hormone has an effect on bone cells and can impact the body through the endocrine system.
It has been known that in order to develop rheumatoid arthritis it was most likely obtained through genetic factors rather than the environment or lifestyle. Each individual gene can contribute to the overall development of this disease. One gene that is a factor for rheumatoid arthritis development is the HLA-DRB1 gene. When this gene is paired with other variations of the gene then the likelihood of developing RA are
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Infectious organisms are beginning to become a main contributor for the inflammation. This in turn begins to target the synovial joints where the pathogenic T cells, Th1 and Th17, both have a significant part. TNFa, tumor necrosis factor, contributes to the inflammatory process because it contains an array of “proinflammatory” effects. Proinflammatory stimulates the process inflammation effects. A TNF inhibitor, found in immunotherapeutic medicine, is needed to suppress and reduce the inflammatory process that occurs. If a patient with rheumatoid arthritis has a deficiency or an abundance of TNFa their symptoms may have greater infection and arthritis. TNFa then promotes the cytokines, IL-1 and IL-6 and then stimulates IL-8, MCP-1, MIP-1α, and RANTES, the macrophages. The cytokines that are created by the pathogenic T cells are known to play a role in the initiation of rheumatoid arthritis. An immunotherapeutic medicine that contains the inhibitor will block TNFa and in turn prevent the inflammation process. T helper 17 cells also play a role in the inflammation process in joints and tissues. TH17 is closely associated and regulated by

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