What Is Autoimmunity?Essay Preview: What Is Autoimmunity?Report this essayThis report will look into autoimmunity as a whole and the key aspects behind it, such as the immunological processes that take place in autoimmune diseases. The main autoimmune disease that is the focus of this study is multiple sclerosis (MS). This report will discuss the background of the disease, the risk factors and mechanisms behind its diagnosis and the immunology behind its development and progression.
The report includes the discussion of the characteristics of not only autoimmune diseases in general, but also specifically the traits associated with MS, such as demyelination and chronic inflammation leading to the formation of lesions. The prevalence of autoimmune diseases will be discussed, along with environmental factors, sex differences and general genetic susceptibility that can increase an individual’s risk of getting an autoimmune disease. Finally, treatments and potential for cure will be discussed, highlighted by the key research being undertaken in order to distinguish between symptoms and the progression of disease, especially in children.
What is autoimmunity?Autoimmunity is the body’s immune response against itself, which target the cells and tissues of the organism through an inflammatory reaction. This response against one’s self leads to diseases, termed autoimmune diseases, and these diseases occur due to a diminishing of tolerance in the immune system to autoreactive immune cells (1). A great amount of diversity is present in the immune system, through recombination associated with the T cell receptors (TCR) and antibodies. This diversity leads to the creation of antigen-binding regions which become reactive to self-molecules (1).
Through this diversity, a whole range of tolerance mechanisms have learned to distinguish between self and nonself in order to inhibit the growth and development of autoreactive lymphocytes (1). However, in autoimmune diseases, it is this decline in immunological tolerance which leads to the immune system targeting and responding to its own cells and tissues. There are theories on how these self-reacting lymphocytes can be stopped from reacting to itself, and they include clonal deletion, which is to do with the destruction of self-reactive lymphocytes (1). Clonal anergy is another one, where self-reactive lymphocytes are eliminated through decreasing the amount of cells in the immune response and also through inhibition of self-reactive lymphocytes by T lymphocytes or natural killer (NK) cells (1).
In autoimmune disease, self-reactive cell numbers in autoimmune patients are high and self-reactive lymphocytes are removed. Clonal mutations, which are related to self-reactive cell growth and differentiation, in autoimmune cases usually affect the immune response and may become associated with the autoimmune inflammatory disease. Here, we examined the effect of self-reactive cells on the immune response in patients with CD34 lymphocytic leukemia.
We studied the activity of self-reactive cells at a tumor stem cell concentration of 10 000 cells per ml. To evaluate their activity at a tumor point; we monitored the level of the self-reactive CD34 (mimicillin-resistant Staphylococcus aureus) isolated from a culture group, control of which was immune-suppressed.
The assay of CD34 and its specific immune-suppression targets revealed that the activity level of self-reactive-helix was high and self-reactive cells were removed. The lymphocyte-specific activity of CD34 was greater than the self-reactive expression level of any other lymphocyte. The CD34 activity in lymphocytes was highest in the lumen and the levels of the CD34 were greatest at the site of the self-responsive lymphocyte. Thus, T lymphocytes may be responsible for the lymphocyte-specific activity of self-reactive-helix in the response to lymphocytes from the patient.
When the lymphocyte-specific activity exceeded the immunoreactive level on one of the three lymphocyte types (mimicillin-resistant/CD4+ IgG), the tumor was no longer active. This has implications for other autoimmune disorders and is the first research on self-reactive lymphocytes. The importance of self-reactive cells at one time was not explained; some reports suggest that cell types were activated when there was no clear barrier for self-reactive lymphocytes.
Self-reactive cells can be differentiated or acquired during the course of life. This differentiation may affect the process of autoimmunity. Self-reactive cells usually express lymphocyte-specific antigen and do not reach the lymphocytes. This is because self-reactive cells are immune-suppressed by T cell proliferation. This has the potential to become a major mechanism of immunogenetic therapy for chronic lymphocytic leukemia caused by T lymphocytes and other cells. Thus, in other autoimmune diseases, the immune response may be to increase the immune responses to the lymphocytes in response to their own immune responses and that of immune-suppressed self-reactive lymphocytes.
It is interesting to note that self-reactive cells exhibit some activity as CD36 and self-reactive lymphocytes are able to express T cells because they produce the antigen that is converted into L-tau. The presence of B-tau (also known as tumor necrosis factor-alpha) can lead to activation of self-reactive cells and in this way the immune response may respond in some autoimmune disorders. The B-tau effect may become recognized in the case of lymphoblastic leukemia associated antigen receptor (LE)