Antigens, Antibodies, and the Immune Response - Essay Example

Antigens, Antibodies, and the Immune Response Introduction The body has its own inherent immune or defence system. In times of possible exposure tobacteria, virus, or other infectious organisms, the body’s defence system is activated. With a strong immune system, the body can naturally resist and resolve infections; however where the immune system is compromised or if the infectious organism cannot be managed by the body’s innate immune system, other symptoms often manifest. These symptoms present as the symptoms of a disease which may have to be managed through antibiotics and other medications. Ideally, however, the body has its inherent defence system which can help reduce the impact of disease on the body. This essay shall discuss antigens, antibodies, and the immune response, including what can happen when a patient has an immune reaction to a blood transfusion. Body First and foremost, the skin itself is the body’s first line of defence. The skin defends the body as it makes it impenetrable to organisms (Kauffman, et.al., 2002). The oil and sweat glands of the skin helps prevent the growth of microorganisms; moreover, sweat has lysozymes which then break down bacterial cell walls. Aside from the skin, the digestive and respiratory tracts also have natural defence mechanisms (Raven, 2006). The cells lining these tracts contain bronchi and bronchioles where mucus is secreted and where microorganisms are then trapped. They are then naturally expelled through coughing, sneezing, vomiting, and diarrhoea. The second line of defence of the body is the cellular level line of defence. Such line of defence includes cells of the body which mostly function for the specific management and elimination of microorganisms (Gorbach, et.al., 2003). The macrophages are the large and irregularly shaped cells. They usually eliminate microbes by ingesting them using the process of phagocytosis. In the macrophage, the lysosome is fused with the bacteria and the microbe is then killed with free radicals in significant quantities released (Raven, 2006). Macrophages also consume viruses and dust particles. They are located in the extracellular fluid and their actions support the actions of other parts of the body, mostly the spleen and the bone marrow. The neutrophils are another type of cell which helps fight off microorganisms (Hornef, et.al., 2002). These are leukocytes which ingest and then kill bacteria, also applying the process of phagocytosis. They also release chemicals which kill the bacteria. The natural killer cells do not directly attack the microorganisms. They attack the cells of the body which has been infected. They create a hole in the membrane of the target cell, allowing water to enter the target cell (Raven, 2006). The cell then expands and is destroyed. The complement system also supports the chemical defence system. This covers different proteins which are floating in the plasma. As they encounter bacteria, the bacteria is attacked and destroyed. Interferons also have a function to play in the body’s defence system (Gross, et.al., 2008). These interferons include the alpha, beta, and gamma interferon. These cells are messengers, also acting to protect the normal cells from infection. The alpha and beta interferons prevent the increase of the virus with the gamma interferon mostly acting in reaction to infection and cancer (Gross, et.al., 2008). The inflammatory reaction is often localized with injured cells releasing chemicals signs. The chemicals then cause the blood vessels to dilate, also promoting blood flow to the site infected or injured (Janssen, et.al., 2005). As a result, the area infected becomes red and warm. The capillaries at the site of infection become more permeable, often leading to oedema. The phagocytes then move into the extracellular fluid and attack the bacteria. The neutrophils are usually the first to arrive at the site of infection; they immediately release chemicals which kill bacteria in the immediate vicinity (Janssen, et.al., 2005). Pus often seen in some infections usually includes dead or dying pathogens, the neutrophils, as well as tissue cells. Monocytes also arrive and turn into macrophages consuming the pathogens (Raven, 2006). Macrophages which are exposed to microbes often release a regulatory molecule known as the interleukin-1. This interleukin-1 including other pyrogens affects the neurons in the hypothalamus, leading to an increase in body temperature (Gal, et.al., 2005). This signals the fever. Fever affects the defence system by further stimulating phagocytosis, thereby allowing the spleen to store iron, and decreasing iron in the blood which is usually needed by the bacteria in order to multiply (Raven, 2006). Some fevers which are highly elevated can however be dangerous as they inactivate the enzymes needed by the body. High fevers are 40 degrees and above are also very much dangerous to the body. Some key concepts of specific immunity include the antigen, the antigenic determinant sites, and the antibodies (Ganz, 2003). The antigens are molecules which often trigger the specific immune response. They are large molecules, same as proteins, and are seen at the surface of pathogens. These antigens have different parts and each part often triggers specific immune reactions. The different parts are considered the antigenic determinant sites and these sites have different antigen responses. The lymphocytes include receptor proteins which recognize antigens and direct specific immune responses against the cell which has the antigen. Lymphocytes known as B cells react to antigens by creating proteins or antibodies (Gans, 2003). These proteins are released into the blood, thereby creating humoral immunity. Other lymphocytes like the T cells do not release antibodies, but directly attack the cells which have specific antigens. Such cells can create cell-mediated immunity. The immune response supports the body by first allowing the individual to have immunity in his exposure to the pathogen (Raven, 2006). This would be known as the acquired immunity. Also, individuals can also secure immunity by being incorporated antibodies from other individuals. This is known as passive immunity, as happens usually during birth with the mother passing on some of her antibodies to her new born through the placenta. The immune defence of the body includes actions from the leukocytes which include the neutrophils, eosinophils, basophils, and monocytes. Lymphocytes (T cells and B cells) are also part of the immune response of the body (Raven, 2006). The T-cells manage the cell-mediated reactions with the C cells handling the humoral response. The T-cells can identify pathogens and with millions of these cells made, each have specialized functions in recognizing specific antigens. The inducer T cells manage the T cell development in the thymus; the helper T cells assist in the immune reaction; the cytotoxic T cells lyse cells affected by viruses; and the suppressor T cells resolve or end the immune response (Mandell, et.al., 1995). The B cells do not traverse the thymus, they mature at the bone marrow. They act mostly on foreign antigens and on exposure to such antigens, it proceeds to divide rapidly, later being differentiated into plasma cells and memory cells. The plasma cells create antibodies which mark the antigen for destruction (Raven, 2006). The cell-mediated immune response by the T cells gives protection to the body from the virus and from cancer, as it then targets the abnormal or virus-ridden cells. As the helper T-cell which allows for this response is presented with the foreign contaminant a complicated series of actions follow (De Smet and Contreras, 2005). A significant aspect of the process would be the release of the autocrine regulatory molecules of the cytokines or the lymphokines from the lymphocytes. On its release, it is defined based on its reaction. However as each cytokine have different reactions, the names can be a misnomer. The interleukin term seems more appropriate. Interleukin 1 for instance is released by macrophages and can trigger the T cell system (De Smet and Contreras, 2005). The B-cell stimulating factor or interleukin-4 is released by T-cells and is needed for proliferation as well as clone development of the B cells. Interleukin-2 comes from the helper T cells. They are essential in activating cytotoxic T lymphocytes. As macrophages identify and react to foreign antigens, they also release interleukin-1 which then causes cell division and the increase of T-cells. As the helper T cells have been increased, gamma interferon also assists in the macrophage activity (Wright, 2005). Moreover, the helper T-cells also releases interleukin-2 which then triggers the increase of the T cells which have specific functions. The cytotoxic T cells are able to destroy the infected cells only if these cells indicate foreign antigen alongside the MHC-1 proteins. The B cells also react to the helper T cells which are activated by interleukin-1 (Raven, 2006). They also have receptor proteins and are able to identify the invading organisms including the cytotoxic T cells. They mark these for destruction by other cells in the body, including the natural killer cells. Antibodies are proteins and are included in a class known as the immunoglobulins which have further subclasses including the IgM which is the first kind of antibody released during the initial infection. They help support agglutination, making antigen stick together. The IgG is the primary antibody in the blood plasma and is released as a secondary response (Turvey, 2010). The IgD are receptors for antigens within the B-cell surface. Their functions are not known. The IgA is the antibody for external secretions including saliva and milk. The IgE supports the secretion of histamine and other agents which also attack the antigen (Turvey, 2010). Microorganisms are a usual part of a person’s life and microorganisms may lead to diseases. Most of these organisms are destroyed by the body’s innate immune system. In order to recognize pathogens, the innate and adaptive immune systems are able to differentiate between the self and nonself pathogens (Turvey, 2010). Differences are however seen in how they differentiate the pathogens. Innate immunity is dependent on various receptors as well as proteins which are then incorporated in the germline, able to identify the common qualities for the pathogens. Adaptive immunity on the other hand includes a process where the somatic cell gene is rearranged to create various antigen receptors which can distinguish between the related molecules. However, the innate immune system sufficiently differentiates between the host cells as well as the pathogens, allowing for initial defences and also affecting the initiation of the adaptive immune reactions (Beutler, 2004). The significance of inherent immunity is observed in the fact that issues relating to the components which are not common can lead to a greater vulnerability to infection, even with an already intact adaptive immune mechanism. The response to new pathogen often unfolds in three stages. At first, as pathogens are able to enter the physical anatomic barriers of the host, the innate immune system reacts quickly. Such defences cover different types of soluble molecules in the blood, the cells, and secretions often immediately set out to kill the pathogen and weaken the impact of such pathogen (Beutler, 2004). The antimicrobial enzymes including the lysozyme then proceed to break down the bacterial walls with peptides including the defensins dissolve the cell membranes. The plasma proteins or the complement system target the pathogens for the lysis and the phagocytosis of the cells of the immune system including the macrophages. After the second phase, the innate immune cells detect the presence of the pathogen and are then activated triggering different effector defences which would then fight off the infection (Pancer and Cooper, 2006). On their own, both soluble and cellular components create long-term protective immunological memory. Only where the infectious microbes enter these lines of defence would reactions be produced to cause an adaptive immune reaction which is the third reaction to the pathogen. This can expand the antigen-specific lymphocytes which specifically target pathogens and form memory cells which secure sufficient and long-lasting immunity (Turvey, 2010). Pathogens are different depending on their lifestyles, or their surface structure; as a result, different defensive reactions from the immune system are needed (Turvey, 2010). The immune response to invading microbes goes through several stages covering the innate, the induced innate, and the adaptive immunity. The initial stage covers processes which are prepared to resist infectious organisms at any given time. The skin surface act as physical barriers, as was previously mentioned and such surface also has special strategies to resist infection (Pulendran and Ahmed, 2006). The surfaces have barriers for and protect the body against colonization from bacteria and virus. Defence mechanisms also help prevent pathogen adherence as well as secretion of antimicrobial and peptides. The antimicrobial peptides are often inactive proproteins which call for proteolytic steps to manage activation, usually generating cationic peptides which have amphipathic qualities which are able to disturb the cell membrane of microbes (Turvey, 2010). The antimicrobial lectins which are able to identify the glycans in specific pathogens and are able to disrupt microbial cell walls also call for proteolytic room for activity. The reactions of the antimicrobial enzymes usually bind to the identified carbohydrate structures. In effect, these soluble molecular reactions are pattern recognition receptors as well as effector molecules, signifying simple forms of immunity (Turvey, 2010). During blood transfusions however, the body may have immune reactions. Hemolytic reactions are considered serious complications which may follow blood transfusions (Yi Bin, 2010). The red blood cells during transfusion can be damaged by the immune system of the patient. Blood has different types: A, B, AB, and O. The immune system is able to differentiate its blood cells other blood cells of other people. Where other blood cells are introduced in the body, the immune system may have the antibodies against such blood cells (Yi Bin, 2010). The antibodies would likely attack the blood cells which the immune system may not recognize. Blood cells are also grouped into Rh factors (Ting, 2005). Those with Rh factors are considered Rh positive, those without are known as Rh negative. The Rh negatives have antibodies against the Rh factor if they would be transfused with the Rh positive blood. Other factors also classify blood cells, aside from ABO and Rh. Blood from transfusions must match one’s own blood. As such, the body does not contain antibodies against blood received (Yi Bin, 2010). Most times, no issues are seen where compatible blood qualities are transfused. For the incompatible groups, an immune response is observed and can cause serious transfusion reactions (Ting, 2010). The immune system would then attack the blood transfused, damaging and destroying them. The immune reactions are primarily attributed to the sensitization of the blood cells donated, the platelets, or the plasma proteins (Yi Bin, 2010). With less frequency, the cells transfused cause the immune response against the recipient and immune complications may be classified into either haemolytic or non-hemolytic reactions. The haemolytic reactions often include blood cells attacked by the recipient’s antibodies. Hemolysis is an acute and uncommon reaction. It is also usually delayed (Yi Bin, 2010). The acute haemolytic reaction is also caused by the ABO blood type incompatibility (Ting, 2005). Human errors often cause this reaction as when blood of a different type is given to a patient. Most times, the operating room is the site of this medical error with anaesthesiologists often attributed with fault for such errors. The reaction has been seen in about 1 in 25,000 transfusions, and has sometimes led to severe reactions and 50% reported deaths from the transfusion (Ting, 2005). The amount of blood given to the patient often determines the severity of the immune reaction. The patient suffering from such reaction may manifest chills, fever, chest pain, and flank pain. These reactions are observed for those who are awake. For those under anaesthesia, reactions seen include increase in temperature, tachycardia, hypotension, DIC, renal shutdown, and shock (Yi Bin, 2010). In order to manage acute haemolytic reactions, the transfusion must immediately be stopped and the blood pocket checked for the type of blood (Ting, 2005). Blood from the recipient must then be tested for haemoglobin in plasma with compatibility testing including coagulation evaluation. A foley catheter must then be inserted to check for blood in the patient’s urine (Ting, 2005). Diuretics using mannitol must be administered. As rapid blood loss is observed, platelets and fresh frozen plasma may be necessary (Ting, 2005). Conclusion The body’s immune system includes a complicated mechanism which helps ensure the body’s homeostasis. From the skin to the cells, the body is able to prevent infection and is able to reduce the impact of diseases. The skin is the first line of defence of the body as it serves as the physical barrier against macro-organisms and bacteria or harmful viruses. The blood cells contain the white blood cells which serve as the cellular defence of the body against bacteria and other viruses. The respiratory and digestive system has mucous membranes which help catch and expel the bacteria out of the body. The immune system includes different phases which eventually help reduce the impact of microbes into the body. Blood transfusions can cause immune reactions especially where the wrong blood type is introduced into the body or there is Rh incompatibility between the recipient’s and the donor blood. The key to management under these conditions would be to stop the transfusion, recheck the blood pack labels and the patient’s reaction to the blood transfusion. Eliminating the wrong or incompatible blood from the patient’s body is crucial to their survival. Diuretics are therefore part of the treatment including early intervention. References Beutler, B., 2004. Innate immunity: an overview. Mol Immunol, 40:845–859. De Smet, K., and Contreras, R., 2005. Human antimicrobial peptides: defensins, cathelicidins and histatins. Biotechnol. Lett, 27:1337–1347. Gál, P., Harmat, V., Kocsis, A., Bián, T., Barna, L., Ambrus, G., and Végh, B., 2005. A true autoactivating enzyme. 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