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Applied Immunology: Hypersensitivity - Essay Example

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As the paper "Applied Immunology: Hypersensitivity" tells, the first type of hypersensitivity reaction is mediated by IgE immunoglobulins. Allergens when enter the body, bind to IgE immunoglobulins which then bind to specific receptors resulting in degranulation and release of mediators…
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Applied Immunology: Hypersensitivity
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The major result of type 1 hypersensitivity reaction is Anaphylaxis which can lead to shock and death (Abbas, 2009) (Bendixen, 1971).

            Type 2 hypersensitivity reaction is mainly mediated by IgG antibody/Immunoglobulin. Foreign substances such as drugs etc. when enter the body bind to IgG antibodies present on the surface of many cells e.g. RBCs. These antigen-antibody complexes attract the cells of the immune system towards them which then attack these cells and destroy them. Rh incompatibility in erythroblastosis fetalis is one example of type 2 hypersensitivity reactions (Abbas, 2009).

            Type 3 hypersensitivity is mediated by immune complexes which are formed when an antigen enters the body and binds with antibodies. These immune complexes are usually phagocytosed by WBCs but when phagocytosed they accumulate at different sites in the body such as kidneys and joints leading to an inflammatory reaction against them e.g. glomerulonephritis and arthritis (Bendixen, 1971).

Type 4 is a delayed hypersensitivity reaction caused by subsequent exposure of the body to certain allergens causing the formation of T-cells and their reaction against that specific antigen. When the body is exposed to an antigen, a specific immune response is activated against it and the formation of T-cells is a part of that immune response. In addition to the formation of T-cells, memory T-cells are also formed. These memory T-cells act immediately when there is subsequent exposure of the body to that specific antigen resulting in a delayed type of hypersensitivity reaction (Parkes, 1994) (Bordow, 2005).

Asthma and its early and late phase reactions:

            Asthma is a type 1 hypersensitivity reaction that is caused by the entry of allergens into the respiratory system leading to the activation of IgE antibodies (Silverstein, 1997). IgE antibodies then bond to the allergens and get attached to the receptors on the surface of the mast cells. These mast cells release histamine which is a strong bronchoconstrictor leading to the constriction of bronchioles causing asthma (Bordow, 2005) (Murphy, 1998). Asthma can cause respiratory failure leading to decreased oxygen supply to the brain causing anoxia and may even lead to coma and death of a person in case of anoxic brain injury.

            The development of asthma is usually divided into two phases

  • Early phase reactions
  • Late phase reactions

Early phase Reactions:

            This phase usually starts immediately after the body is exposed to allergens. As explained in type 1 hypersensitivity reaction, this phase starts when an allergen enters the human body and binds with IgE antibodies. This allergen antibody complex moves towards histamine-releasing cells and mast cells and gets attached to specific antigen receptors on the cell membrane. Degranulation of mast cells occurs and histamine is released from them. This released histamine which is one of the main mediators of type 1 hypersensitivity reaction moves towards its receptors, binds with them, and acts as a potent bronchoconstrictor (Peacock, 2000). Immediate symptoms of asthma develop in the early phase reaction. These symptoms are itchy eyes, runny nose, and shortness of breath. These symptoms mainly shortness can be eradicated by the use of strong bronchodilators (Barnes, 1997). Bronchodilators such as epinephrine and other beta-agonists act at specific beta-2 receptors in the bronchioles opposing the bronchoconstriction effects of histamine and causing immediate bronchodilation as well as alleviating other symptoms.  

Late Phase Reactions:

            Late phase reaction of asthma is mainly a cellular inflammatory reaction and usually develops after 3-10 hours of initial exposure to the allergen. The late-phase asthmatic response is mainly due to the movement of immune cells of the body toward the site of the reaction. When basophils and mast cells release histamine and other mediators, they also release chemotactic factors which when released cause the movement of immune cells such as eosinophils toward the site of reaction and causing an inflammatory response (Levy, 2006).

            Late-phase reactions of asthma are supposed to be caused by the cells which are not a part of the respiratory system but move towards it when chemical mediators are released to find and destroy the allergen resulting in a hyperactive immune system. Cells taking part in late-phase reactions of asthma usually include eosinophils, basophils, and T cells which then cause the release of inflammatory factors such as leukotrienes and interleukins. These inflammatory substances when released cause the movement of more immune cells towards the respiratory system resulting in inflammation of the cells of the respiratory system (Durham, 1987). Continuous inflammation of the respiratory system, if not treated at the right time or left untreated can deteriorate the symptoms leading to worsening of the condition and irreparable injury to the cells of the respiratory system. Conditions such as emphysema are a common complication of chronic asthma.  

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