Appreciatively, recent clinical research such as HLA tetramers and microarray techniques are likely to provide a clinical application for hypersensitivity reactions.
Hypersensitivity reactions (HR) are immune responses that are exaggerated or inappropriate against an antigen or allergen. Coombs and Gell classified hypersensitivity reactions into four forms. Type I, type II, and Type III hypersensitivity reactions are known as immediate hypersensitivity reactions (IHR) because they occur within 24 hours. Antibodies including IgE, IgM, and IgG mediate them.
Type I (immediate) hypersensitivity reactions
Type I (immediate) hypersensitivity reactions (anaphylactic type) are characterized by IgE-dependent release of chemical mediators from mast cells and basophils. Cross-linking of IgE bound to the antigen to IgE Fc receptors on the surface of mast cells and basophils causes degranulation. This binding triggers release of chemical mediators that include histamine and heparin; eosinophil chemotactic factor; leukotriene B4 and neutrophil chemotactic factor; and prostaglandin D4, platelet-activating factor (PAF), and leukotrienes C4 and D4. The influx of eosinophils amplifies and perpetuates the reaction. Effects may be systemic (anaphylaxis, as for example due to bee stings or drugs) or localized (food allergies, atopy, and asthma).
Type II hypersensitivity reactions
Type II hypersensitivity reactions (antibody-mediated) are mediated by IgG or IgM antibodies directed against a specific target cell or tissue. Reactions can take several forms.
In complement-dependent cytotoxicity, fixation of complement results in osmotic lysis or opsonization of antibody-coated cells; examples include auto-immune hemolytic anemia, transfusion reactions, and erythroblastosis fetalis.
In antibody-dependent cell-mediated cytotoxicity (ADCC), the cytotoxic killing of an antibody-coated cell occurs; an example is pernicious anemia. Antireceptor antibodies can activate or interfere with receptors; examples include Graves disease and myasthenia gravis.
Type III hypersensitivity reactions
Type III hypersensitivity reactions (immune complex disease) are characterized by the formation of in situ or circulating antibody-antigen immune complexes, which deposit in the tissue resulting in inflammation and tissue injury. Examples include serum sickness, systemic lupus erythematosus (SLE), and glomerulonephritis.
Type IV hypersensitivity reactions
Type IV hypersensitivity reactions (cell-mediated type) are mediated by sensitized T lymphocytes. In delayed-type hypersensitivity, CD4+ TH1 lymphocytes mediate granuloma formation; examples include the PPD skin test and tuberculosis.
In cytotoxic T-cell–mediated hypersensitivity, CD8+ T-cell lymphocytes destroy antigen-containing cells; examples include type 1 diabetes, virus-infected cells, an immune reaction to tumor-associated antigens, and graft rejection.
Hypersensitivity reactions to food, insect venom, spore, and drugs are not rare. Appreciatively, recent clinical research such as HLA tetramers and microarray techniques are likely to provide a clinical application for hypersensitivity reactions.