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This Concept Map, created with IHMC CmapTools, has information related to: Answers_Hypersensitivities, Delayed hypersensitivity is the same mechanism as cell-mediated immunity. T8-lymphocytes become sensitized to an antigen and differentiate into cytotoxic T-lymphocyteswhile effector T4-lymphocytes become sensitized to an antigen and produce cytokines. results TH1 cells activate macrophages causing the production of inflammatory cytokines and extracellular killing by the macrophages leading to tissue damage., The antigen/antibody complexes then activate the classical complement pathway. results Aggregation of platelets, resulting in more inflammation and the formation of microthrombi that block capillaries., Type IV (Delayed hypersensitivity) mechanism Delayed hypersensitivity is the same mechanism as cell-mediated immunity. T8-lymphocytes become sensitized to an antigen and differentiate into cytotoxic T-lymphocyteswhile effector T4-lymphocytes become sensitized to an antigen and produce cytokines., Delayed hypersensitivity is the same mechanism as cell-mediated immunity. T8-lymphocytes become sensitized to an antigen and differentiate into cytotoxic T-lymphocyteswhile effector T4-lymphocytes become sensitized to an antigen and produce cytokines. results TH2 cells produce interleukin-4 (IL-4) and interleukin-5 (IL-5) to promote extracellular killing by eosinophils and causing tissue damage., Late phase allergic reactions may begin several hours after exposure to antigen. physiologic changes from inflammatory agents Dilation of blood vessels. This causes local redness (erythema) at the site of allergen delivery. (If dilation is widespread, this can contribute to decreased vascular resistance, a drop in blood pressure, and shock.), These small complexes lodge in the capillaries, pass between the endothelial cells of blood vessels - especially those in the skin, joints, and kidneys - and become trapped on the surrounding basement membrane beneath these cells. next The antigen/antibody complexes then activate the classical complement pathway., The antigen/antibody complexes then activate the classical complement pathway. results Massive inflammation, due to complement protein C5a triggering mast cells to release inflammatory mediators, Either IgG or IgM is made against normal self antigens as a result of a failure in immune tolerance, or a foreign antigen resembling some molecule on the surface of host cells enters the body and IgG or IgM made against that antigen then cross reacts with the host cell surface. examples AB and Rh blood group reactions. Autoimmune diseases such as: Rheumatic fever where antibodies result in joint and heart valve damage; Idiopathic thrombocytopenia purpura where antibodies result in the destruction of platelets; Myasthenia gravis where antibodies bind to the acetylcholine receptors on muscle cells causing faulty enervation of muscles; Goodpasture's syndrome where antibodies lead to destruction of cells in the kidney; Multiple sclerosis where antibodies are made against the oligodendroglial cells that make myelin, the protein that forms the myelin sheath that insulates the nerve fiber of neurons in the brain and spinal cord. Some drug reactions., Hypersensitivities Types of Hypersensitivities Type III (Immune complex-mediated), Type I (IgE-mediated or anaphylactic-type) mechanism IgE is made in response to an allergen. (In allergic individuals, the levels of IgE may be thousands of times higher than in those without allergies.), Late phase allergic reactions may begin several hours after exposure to antigen. physiologic changes from inflammatory agents Stimulation of mucous secretion. This leads to congestion of airways., Late phase allergic reactions may begin several hours after exposure to antigen. physiologic changes from inflammatory agents Constriction of bronchial airways. This leads to wheezing and difficulty in breathing., Delayed hypersensitivity is the same mechanism as cell-mediated immunity. T8-lymphocytes become sensitized to an antigen and differentiate into cytotoxic T-lymphocyteswhile effector T4-lymphocytes become sensitized to an antigen and produce cytokines. results CTLs use their TCR/CD8 to bind to peptide epitopes bound to MHC-I on infected cells or normal cells having cross-reacting epitopes and kill them through apoptosis., Late phase allergic reactions may begin several hours after exposure to antigen. physiologic changes from inflammatory agents Increased capillary permeability. This causes swelling of local tissues (edema). (If widespread, it can contribute to decreased blood volume and shock.), The antigen/antibody complexes then activate the classical complement pathway. results MAC lysis of surrounding tissue cells, due to the membrane attack complex., IgE is made in response to an allergen. (In allergic individuals, the levels of IgE may be thousands of times higher than in those without allergies.) next The Fc portion of IgE binds to the surface of mast cells and basophils., Type I (IgE-mediated or anaphylactic-type) treatments When very dilute allergen is given by injection, it stimulates the production of IgG and IgA. IgG and IgA then act as blocking antibodies to bind and neutralize much of the allergen in secretions before it can bind to the deeper cell-bound IgE on the mast cells in the connective tissue.The shots also appear to suppress production of IgE by inducing tolerance and/or by activating T8-suppressor cells., The antigen/antibody complexes then activate the classical complement pathway. results Influx of neutrophils, due to complement protein C5a, resulting in neutrophils discharging their lysosomes and causing tissue destruction through extracellular killing and causing further inflammation., The Fc portion of IgE binds to the surface of mast cells and basophils. early phase When the allergen cross-links the Fab portions of the mast cell-bound IgE, this triggers histamine release by the mast cell, a process called degranulation, and the synthesis of other inflammatory mediators such as platelet-activating factor, leukotrienes, bradykinins, prostaglandins, and cytokines that contribute to inflammation. These agents cause the early phase of allergic reactions that appears within minutes after exposure to the antigen., Hypersensitivities immediate versus delayed Immediate hypersensitivities refer to humoral immunity (antigen/antibody reactions) causing harm.
