Hypersensitivity may be defined as an exaggerated or inappropriate immune response causing tissue damage. Hypersensitivity reactions are generally classified into 4 types (types I to IV) although this may be considered an over simplification and more than one type can often be postulated for a patient's hypersensitivity. In each of the 4 types, prior sensitisation of the patient to the specific antigen is required. The term 'allergy' by definition originally covered all types of hypersensitivity reactions as well as the induction of immunity in an individual. Nowadays, the term is more commonly applied to type I hypersensitivity reactions.
Type I, immediate hypersensitivity reactions occur after exposure to an antigen (the allergen) in a sensitised subject; that is, one in whom the initial exposure to the antigen has caused the production of specific antibodies, mainly IgE (immunoglobulin E), which are bound to the surface of mast cells and basophils. At subsequent exposure, antigen binds to antibody resulting in degranulation of mast cells and basophils with release of mediators. These include preformed mediators such as histamine and chemotactic factors, and newly synthesised mediators such as leukotrienes, platelet-activating factor, and prostaglandins. Although type I reactions are usually described as being acute and short-lived, clinically there may often also be a late-phase and more prolonged reaction affecting the skin and bronchi. Examples of type I hypersensitivity reactions include allergic conjunctivitis, allergic rhinitis, urticaria and angioedema, and anaphylactic shock.
Type II, cell-surface hypersensitivity reactions are caused by the interaction of circulating antibodies, mainly IgG (immunoglobulin G) and IgM (immunoglobulin M), with antigens that are on the surface of specific cells or tissues. This interaction results in activation of complement and of phagocytic and killer cells leading to cell damage or lysis. Type II reactions are responsible for blood transfusion reactions, some drug-induced blood disorders, and many auto-immune disorders.
Type III, immune complex hypersensitivity reactions, are caused by the interaction of fixed or circulating antigens with circulating antibodies, mainly IgG and IgM (either soluble or particulate), resulting in formation of immune complexes. The immune complexes trigger a variety of inflammatory processes including complement activation, mediator release from mast cells and basophils, and platelet aggregation. Examples of type III reactions include serum sickness, some auto-immune and neoplastic disorders, type 2 lepra reactions (see Leprosy, and reactions, particularly in the lung, to some particulate antigens such as micro-organisms.
Type IV, cell-mediated or delayed hypersensitivity reactions, are caused by interaction of an antigen with sensitised T-lymphocytes; lymphokines are released by T-lymphocytes and inflammation ensues. Type IV reactions usually occur at least 24 hours after contact with the antigen. A type IV reaction is responsible for tuberculin reactions used for sensitivity testing, contact dermatitis, and some reactions to chronic infectious disease for example type 1 lepra reactions.
An anaphylactoid (pseudoallergic) reaction produces similar symptoms to those of anaphylaxis, but is caused by direct release of histamine provoked by an unclear, non-immune mechanism. There is thus no requirement for prior exposure to the triggering factor, commonly a drug.
Type I, immediate hypersensitivity reactions occur after exposure to an antigen (the allergen) in a sensitised subject; that is, one in whom the initial exposure to the antigen has caused the production of specific antibodies, mainly IgE (immunoglobulin E), which are bound to the surface of mast cells and basophils. At subsequent exposure, antigen binds to antibody resulting in degranulation of mast cells and basophils with release of mediators. These include preformed mediators such as histamine and chemotactic factors, and newly synthesised mediators such as leukotrienes, platelet-activating factor, and prostaglandins. Although type I reactions are usually described as being acute and short-lived, clinically there may often also be a late-phase and more prolonged reaction affecting the skin and bronchi. Examples of type I hypersensitivity reactions include allergic conjunctivitis, allergic rhinitis, urticaria and angioedema, and anaphylactic shock.
Type II, cell-surface hypersensitivity reactions are caused by the interaction of circulating antibodies, mainly IgG (immunoglobulin G) and IgM (immunoglobulin M), with antigens that are on the surface of specific cells or tissues. This interaction results in activation of complement and of phagocytic and killer cells leading to cell damage or lysis. Type II reactions are responsible for blood transfusion reactions, some drug-induced blood disorders, and many auto-immune disorders.
Type III, immune complex hypersensitivity reactions, are caused by the interaction of fixed or circulating antigens with circulating antibodies, mainly IgG and IgM (either soluble or particulate), resulting in formation of immune complexes. The immune complexes trigger a variety of inflammatory processes including complement activation, mediator release from mast cells and basophils, and platelet aggregation. Examples of type III reactions include serum sickness, some auto-immune and neoplastic disorders, type 2 lepra reactions (see Leprosy, and reactions, particularly in the lung, to some particulate antigens such as micro-organisms.
Type IV, cell-mediated or delayed hypersensitivity reactions, are caused by interaction of an antigen with sensitised T-lymphocytes; lymphokines are released by T-lymphocytes and inflammation ensues. Type IV reactions usually occur at least 24 hours after contact with the antigen. A type IV reaction is responsible for tuberculin reactions used for sensitivity testing, contact dermatitis, and some reactions to chronic infectious disease for example type 1 lepra reactions.
An anaphylactoid (pseudoallergic) reaction produces similar symptoms to those of anaphylaxis, but is caused by direct release of histamine provoked by an unclear, non-immune mechanism. There is thus no requirement for prior exposure to the triggering factor, commonly a drug.
Martindale: The Complete Drug Reference © 2007 The Pharmaceutical Press.
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