Autoimmunity and risk of cancet Essay Example | Topics and Well Written Essays - 1000 words

Autoimmunity and risk of cancet - Essay Example Discussion Stimulation of T-cell leads to maintained survival of T-cells when stimulated by self-protein MHC. Lymphoproliteration results if T-cell homeostasis is altered. Moreover, in certain circumstances, an interaction between activated T-cells and B-cells (e.g CD40L-CD40 interaction) may lead to autoimmunity (Rose & Mackay, 2006). Sometimes, the presence of self-antigen may become the cause of stimulation of T-cells; this activation is tolerated by phenomenon like anergy or deletion (Mak & Saunders, 2006). It therefore follows that failure to achieve deletion in this scenario may cause an autoimmune process to flourish. Moreover, defectively matured dendritic cells might interact with T-cells to generate a class to T-cells that are directed against self-antigens. Upon infection by a foreign pathogen, T-cells are activated and various clones are generated. Some of these clones can possibly cross-react with self-antigens resulting in transient or permanent autoimmunity (Ohashi, 20 02). In normal cells, the process of production of cells is tightly regulated by a number of very important mechanisms. Moreover, the new cells which are produced become differentiated and specialized to perform the function for which they are produced (Sherwood, 2012). This controlled multiplication of cells when becomes defective leads to the production of cells which are uncontrolled; cells start producing in an uncontrollable fashion. Therefore, due to this type of defective mitotic process, the cells that are produced are 'de-differentiated' and unable to perform their desired function. This results in a neoplasm. Neoplastic tissue demonstrates a growth rate that exceeds the growth rate of normal healthy tissue of the body (Stubblefield & O'Dell, 2009). For this reason, it manifests as a mass which is often referred to as a tumor. Since cancerous cells are not the exact replicas of the normal healthy cells of the body, they fail to mask themselves from the functioning immune sy stem of the body (Brunner & Smeltzer, 2010). Certain signals are 'flagged' on the cell membrane of cancerous cells that invite cells of the immune system to target such cells; therefore in most cases they are destroyed prior to the formation of their clone; cancerous cells are monoclonal in origin (Tobias et al, 2010). Inflammation brings about a number of changes to the vascular and epithelial tissues. Moreover, it affects the function of immune cells. This is the result of a complex interplay of molecules like cytokines, growth factors and chemokines (Jabbour et al, 2009). Furthermore, chronic inflammation due to irritation or infection has been accepted as a cause of cancer. Persistence of inflammation has been related to tumorigenesis and progression of cancer (Coussens & Werb, 2002). Tumor necrosis factor (TNF) plays a vital role in mediating inflammation by causing tissue destruction as well as recovery. The actions of TNF result in fibroblast growth which can destroy blood ve ssels and at the same time contribute to angiogenesis (Kollias et al, 1999). As far as the etiology of cervical cancer is concerned, the causative organism has been identified to be Human Papilloma Virus (HPV). Studies have shown that E6 and E7 oncogenes are incorporated into the genome of the host (Radosevich, 2012; Robertson, 2011; Stanley et al,