Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen.[1] Type I is distinct from type II, type III and type IV hypersensitivities. Show
Exposure may be by ingestion, inhalation, injection, or direct contact. Pathophysiology[edit] Flowchart depicting the pathophysiology of Type I Hypersensitivity reactions [2] In type I hypersensitivity, B cells are stimulated (by CD4+ Th2 cells) to produce IgE antibodies specific to an antigen. The difference between a normal infectious immune response and a type 1 hypersensitivity response is that in type 1 hypersensitivity, the antibody is IgE instead of IgA, IgG, or IgM. During sensitization, the IgE antibodies bind to FcεRI receptors on the surface of tissue mast cells and blood basophils.[3] Mast cells and basophils coated by IgE antibodies are "sensitized". Later exposure to the same allergen cross-links the bound IgE on sensitized cells, resulting in anaphylactic degranulation, which is the immediate and explosive release of pharmacologically active pre-formed mediators from storage granules and concurrent synthesis of inflammatory lipid mediators from arachidonic acid;[4] some of these mediators include histamine, leukotriene (LTC4 and LTD4 and LTB4), and prostaglandin, which act on proteins (e.g., G-protein coupled receptors) located on surrounding tissues.[4] The principal effects of these products are vasodilation and smooth-muscle contraction. Type I hypersensitivity can be further classified into immediate and late-phase reactions. Within minutes of exposure to an antigen, the immediate hypersensitivity occurs, releasing histamines and lipid mediators which are responsible for the initial allergic reaction response. However, about 4-12 hours after antigen exposure, a cough and wheezing may persist in the patient, along with swelling and redness of the skin. This is known as the late-phase hypersensitivity reaction which can last from approximately 1-3 days and is caused by the release of additional mediators from the mast cells and basophils. [5] List of a few mediators released by mast cells in type 1 hypersensitivity and their actions
The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock. Treatment and prognosis[edit]If multiple systems are involved, then anaphylaxis can take place, which is an acute, systemic reaction that can prove fatal. Treatment usually involves adrenaline (epinephrine) because it counteracts anaphylaxis by increasing blood flow and relaxing bronchial muscles that block one’s airways.[7] Antihistamines and corticosteroids are also commonly used in less severe reactions.[8] Examples[edit]Some examples:
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External links[edit]Which type of hypersensitivity reaction causes rapid anaphylaxis?Type I hypersensitivities include atopic diseases, which are an exaggerated IgE mediated immune responses (i.e., allergic: asthma, rhinitis, conjunctivitis, and dermatitis), and allergic diseases, which are immune responses to foreign allergens (i.e., anaphylaxis, urticaria, angioedema, food, and drug allergies).
What is a Type 2 hypersensitivity reaction?Type II hypersensitivity reaction refers to an antibody-mediated immune reaction in which antibodies (IgG or IgM) are directed against cellular or extracellular matrix antigens, resulting in cellular destruction, functional loss, or tissue damage.
What causes Type II hypersensitivity?Type II hypersensitivity reactions (Fig. 46-2) are caused by chemical modification of cell surface or matrix-associated antigens that generates “foreign” epitopes to which the immune system is not tolerant.
What is a Type 4 hypersensitivity reaction?Type four hypersensitivity reaction is a cell-mediated reaction that can occur in response to contact with certain allergens resulting in what is called contact dermatitis or in response to some diagnostic procedures as in the tuberculin skin test. Certain allergens must be avoided to treat this condition.
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