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Aging and immune system The immune system in our human body is to prevent or limit infections. The first line of defense against microorganism is the intact skin and mucous membrane. If microorganism breach this line and enter into our human body, then it will activate the innate immunity to destroy the invaders. The innate immunity can function immediately upon entry of the microorganisms. The ability of this immunity to kill microorganism is not specific. For example, neutrophil can ingest and destroy many different kinds of bacteria.
While the highly specific protection is provided by the adaptive immunity, but it takes several days to become fully function. The two components of the adaptive immune system are cell-mediated immunity and antibody mediated immunity. The cell mediated immunity consists primarily of T-lymphocytes, whereas antibody mediated immunity consists of antibodies and B lymphocytes. One of the most acknowledged consequences of aging is a decline in immune function. While in senior are no means immunodeficient but do not respond efficiently to new or previously encountered antigens.
The effects of aging on the immune system are widespread and affect the rate at which naive B and T cells are produced as well as the composition and quality of the mature lymphocyte pool. As we age, our body gets stiffer and slower year after year, our immune system also becomes slower to respond. This will increases the risk of getting sick and body may heal more slowly because there are fewer immune cells in the body to bring about healing.
Besides, the immune system’s ability to detect and correct cell defects also declines which will result in an increased risk of cancer. It also will developed an autoimmune disorder which the immune system mistakenly attacks and destroys healthy body tissues. According to the author stated, an autoimmune diseases affect approximately 5% of the world population and the age at onset varies widely depending on the disease [1,2]. For example, type 1 diabetes mellitus is considered a childhood and adolescent disease with two peaks of onset, one between ages 5 and 9 and a second between ages 10 and 14 . On the other hand, an adult onset would be considered to be in a range of 25″61 years old .Type 1 diabetes is also known as insulin-dependent diabetes mellitus (IDDM) is a chronic autoimmune disease with a subclinical prodromal period characterized by selective destruction of insulin-producing beta cells in the pancreatic islets which will leading to insulin deficiency. The beta cell damage may be induced at any age, where childhood and late-onset patients are characterized by symptoms like polydipsia, polyuria, and weight loss, but younger patients suffer more from diabetic ketoacidosis and ketosis as the initial presentation [5,6]. In pathologically, type 1 diabetes is autoimmune destruction of pancreatic islets where it infiltrated with lymphocytes, this process known as insulitis. After all beta cells are destroyed, the inflammatory process abates and pancreatic islets are become atrophic. The autoimmune destruction of pancreatic beta cell leads to deficiency of insulin secretion. This loss of insulin secretion that leads to the metabolic derangement associated with IDDM. In addition, the loss of insulin secretion will leads to the abnormal function of pancreatic alpha cell. Furthermore, there is a excessive secretion of glucagon in IDDM patients but normally in condition of hyperglycemia leads to reduces glucagon secretion. However, the patient with IDDM their glucagon secretion is not suppressed by hyperglycemia. Type 1 diabetes is much typically arises in children but it is not a childhood disease. It occurs at every age, in people of every race, and of every shape and size. In fact, there are more adults who have type 1 diabetes than children, although it was previously known as juvenile diabetes. Although type 1 diabetes can appear at any age, it appears at two noticeable peaks which are between 4 and 7 years old and between 10 and 14 years old. In addition, the environmental factors may trigger initial beta cell damage and subsequently accelerate the destructive process which will also leads to type 1 diabetes. The undefined environmental factor are viral infection, where the group coxsackie B viruses are commonly named as putative type 1 diabetes inducing agents. It impaired beta cell function and display different cytolytic effects in pancreatic beta cells with some serotypes being highly cytolytic while others replicating without apparently destroying the cell . When a virus invades the body, the immune system are activate and starts to produce antibodies that fight the infection. T and B cells are in charge of making the antibodies, and then they also help in fighting the virus. The virus has some of the same antigens as the beta cells, then the T cells can actually turn against the beta cells. The antibodies can destroy the beta cells and leads to deficiency of insulin secretion. It needs take a long time for the T cells to destroy the majority of the beta cells, but the original viral infection is what thought to trigger the development of type 1 diabetes. The genes also play a role in type 1 diabetes, some people cannot develop type 1 diabetes; that’s because they don’t have the genetic coding that researchers have linked to type 1 diabetes. Nowadays, scientists have figured out that type 1 diabetes can develop in people who have a particular human leukocyte antigen (HLA) complex. There are several HLA complexes that are associated with type 1 diabetes.The type 1 diabetes develops gradually, but the symptoms may seem to come on suddenly.
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