Autoimmunity and the risk of cancer - Essay Example

Autoimmunity and Risk of Cancer Autoimmunity refers to the lack of capa by organisms to recognise constituent elements of the microorganism constituent, leading to development of immunity against the microorganism’s own tissues and cells. Immune system disorders have been linked with the occurrence of immunodeficiency, a condition which makes the immune system less responsive to life threatening infections. Diseases which present these aberrant responses to immunity are referred as autoimmune diseases. Examples of some known autoimmune diseases include rheumatoid arthritis, diabetes mellitus type 1, and Grave’s disease, among several others. The concept of horror autotoxicus contradicts autoimmunity existence, by stating that the aspect of bodies mounting immune response against their own tissues was abnormal, and linked to human disease (Silverstein 2001). Autoimmunity occurs when the immune system becomes hyperactive and attacks normal cells like foreign cells. Immunological mechanism refers to the collection of human cells which perform the fundamental function of providing immunity to diseases. The mechanism can be defined as the body’s defence mechanism, as it provides the body with resistance from infection by foreign microbes (Singh et al. 2014). Immunological mechanism can be effectively induced within the human body through vaccination process, which introduces disease resistance cells into the body. The defence mechanisms of the human body possess the capability to adapt and recognise pathogens through a period of time. The capability to adapt leaves an immunological memory following initial detection of pathogens. On the other hand pathogens also have adaptive capabilities which make them difficult to detect. The process of acquired or adaptive immunity has been the basis for development of vaccines, for different pathogens. Cancer refers to a malignant neoplasm caused by uncontrollable division and growth of cells, resulting in malignant tumour which invades nearby body parts. Cancer constitutes of numerous diseases which result in unregulated growth of cells within the human body(Penn 1982). Causes of these diseases remain diverse as the diseases with few being understood by medical practitioners. Many factors have been identified as increasing the risk for cancer development, including tobacco use, exposure to radiation, genetic factors, and infections, among many others. The characteristic presence of cancer involves damage to genes, through a combination of factors, consequently causing cancerous mutations of body cells. Cell mutation refers to the genetic change in cells which results in production of genetically different cells. These mutated cells have been identified as some causes of cancer. The immune system performs the function of detecting mutation and subsequently destroying mutated cells before they become cancerous (Beral & Newton 1998). The development of cancer has sometimes been linked with the failure by the immune system to perform this fundamental function. Immune system disorders have been identified as making the system incapable of detecting mutations within many human cells. The failure to detect these cells, and destroy them enables the cells to become cancerous, with time. Deficiency within the immune system has been linked with increased occurrence of cancer occurring among humans. Cancer has been established as resulting from uncontrolled growth of mutated cells within the human body. While this might be true, incapacity by the immune system to provide defence might not be the only cause. The growth of cancerous cells occurs at rates which the immune system cannot destroy these cells. The system therefore becomes overpowered by the spontaneous multiplication of mutated cells. Inflammation cancer, like cervical cancer, results in an inflammation occurring on the skin, which damages some body cells. The mutated cells release chemicals which initiate genetic faults, enabling immune cells to become mutated. Once mutated, the immune system becomes weakened as these cells become infiltrated within the tumour. B cells are lymphocytes occurring with the adaptive immune system of human body. These cells provide immunity through binding specific antigens using manufactured antibodies. The cells are produced in the bone marrow and perform the function of producing antibodies against specific antigens (Dalloul 2009). B cells form memories which are activated upon interaction with antigens, ensuring similar reaction in future regarding the specified antigen. Within the bone marrow, the B cells become tested for auto-reactivity, a mechanism which becomes essential in ensuring the cells do not destroy self-antigens. Cells showing signs of auto-reactivity become destroyed before moving to the lymphatic system. The B cells must become activated before producing antibodies. T cells on the other hand perform a role of assisting other lymphatic cells in immunological processes, like the maturation of B cells. They perform a supportive role within the immune system. These cells perform a fundamental role in destruction of cells deemed to display attributes of antigen fragments (Murphy et al. 2012). These cells are not subjected to central tolerance testing as they are self-tolerance and self-restricted. This characteristic makes them capable of inducing autoimmune diseases into the hosting body. The human body cells which turn into cancerous cells lack the capabilities portrayed by B and T cells. If cancerous cells had mechanisms similar to the lymphatic cells, they would be incapable of undergoing mutation (Porta et al. 2011). The cells would self-destroy upon detection of genetic variations within their constituents. While there is evidence linking immune deficiency with cancer, this applies to specific forms of cancer. Cervical cancer has not been linked with immune deficiency in humans. Autoimmunity has been continuously linked with development of cancer among many individuals. Evidence has however been complicate issue as some treatments to common autoimmunity diseases increase the risk of cancer, and not the disease itself (Volkers 1999). The presence of autoimmune diseases increases the risk of cancer. Many researches have not ascertained this increased risk linkage to treatment method or the autoimmune disease. Existing information between autoimmunity and cancer indicates minimal relationships existing between the two aspects. The mechanism utilised in development of autoimmunity can be identified as being negatively applied in the development of cancerous cells (Neurath & Finotto 2011). While autoimmunity involves self-destruction by cells, development of cancer involves self-transformation of cells, when they come into contact with cancerous cells. the process of development of cancerous cells is marked by self-reactivity characteristic of cells close to cancerous cells within the human body. References Beral, V. & Newton, R., 1998. Overview of the Epidemiology of Immunodeficiency-Associated Cancers. Journal of National Cancer Monographs, (23), pp.1–6. Dalloul, A., 2009. A safeguard against autoimmunity and a shield for cancer cells. Autoimmunity Reviews, 8(4), pp.349–353. Murphy, M.A., O’Leary, J.J. & Cahill, D.J., 2012. Assessment of the humoral immune response to cancer. Journal of Proteomics,, 75(15), pp.4573–79. Neurath, M.F. & Finotto, S., 2011. signaling in autoimmunity, chronic inflammation and inflammation-associated cancer. Cytokine & Growth Factor Reviews, 22(2), pp.83–89. Penn, I., 1982. The occurrence of cancer in immune deficiencies. Current Problems in Cancer, 6(10), pp.1–64. Porta, C., Riboldi, E. & Sica, A., 2011. Mechanisms linking pathogens-associated inflammation and cancer. Cancer Letters, 350(2), pp.250–262. Silverstein, A.M., 2001. Autoimmunity versus horror autotoxicus: the struggle for recognition. Nature immunology, 2(4), pp.279–281. Singh, K., Chang, C. & Gershwin, M.E., 2014. deficiency and autoimmunity. Autoimmunity Reviews, 13(2), pp.163–177. Volkers, N., 1999. Do Autoimmune Diseases Raise The Risk of Cancer? Journal of National Cancer Monographs, 91(23), pp.1992–1993.  Read More