Hypersensitivity is the term used when an immune response results in exaggerated or inappropriate reactions harmful to the host. Generally speaking, hypersensitivity reactions occur in response to external stimuli (antigens) whereas autoimmune reactions (see Chapter 66) occur in response to internal stimuli (antigens). The term allergy is often equated with hypersensitivity but more accurately should be limited to the IgE–mediated reactions discussed later in the section “Type I: Immediate (Anaphylactic) Hypersensitivity.”
The clinical manifestations of these reactions are typical in a given individual and occur on contact with the specific antigen to which the individual is hypersensitive. The first contact of the individual with the antigen sensitizes (i.e., induces the antibody), and subsequent contacts elicit the allergic response.
Hypersensitivity reactions can be subdivided into four main types. Types I, II, and III are antibody-mediated, whereas type IV is cell-mediated (Table 65–1). Type I reactions are mediated by IgE, whereas types II and III are mediated by IgG. The immunologic reactions are summarized in Table 65–1. The clinical manifestations of the hypersensitivity reactions are described in Table 65–2.
TABLE 65–1Immunologic Aspects of Hypersensitivity Reactions |Favorite Table|Download (.pdf) TABLE 65–1 Immunologic Aspects of Hypersensitivity Reactions
|Type ||Antibody or Cell Mediated ||Immunologic Reaction |
|I (Immediate, anaphylactic) ||Antibody (IgE) ||Antigen (allergen) induces IgE antibody that binds to mast cells and basophils. When exposed to the allergen again, the allergen cross-links the bound IgE on those cells. This causes degranulation and release of mediators (e.g., histamine). |
|II (Cytotoxic) ||Antibody (IgG) ||Antigens on a cell surface combine with IgG antibody. This leads to complement-mediated lysis of the cells (e.g., transfusion or Rh reactions) or autoimmune hemolytic anemia. |
|III (Immune complex) ||Antibody (IgG) ||Antigen–antibody immune complexes are deposited in tissues, complement is activated, and polymorphonuclear cells are attracted to the site. They release lysosomal enzymes, causing tissue damage. |
|IV (Delayed) ||Cell ||T lymphocytes activated/sensitized by an antigen release lymphokines upon second contact with the same antigen. The lymphokines induce inflammation and activate macrophages, which, in turn, release various inflammatory mediators. |
TABLE 65–2Clinical Manifestations of Hypersensitivity Reactions |Favorite Table|Download (.pdf) TABLE 65–2 Clinical Manifestations of Hypersensitivity Reactions
|Type ||Typical Time of Onset ||Clinical Manifestation or Disease |
|I (Immediate, anaphylactic) ||Minutes ||Systemic anaphylaxis, urticaria (hives), asthma, hay fever, allergic rhinitis, allergic conjunctivitis, food allergies (e.g., nuts, shellfish, eggs), drug allergies especially penicillin, eczema (atopic dermatitis), bee venom, latex gloves, angioedema |
|II (Cytotoxic) ||Hours to days ||Hemolytic anemia, neutropenia, thrombocytopenia, ABO transfusion reactions, Rh incompatibility (erythroblastosis fetalis, hemolytic disease of the newborn), rheumatic fever, Goodpasture’s syndrome |
|III (Immune complex) ||2 to 3 weeks ||Systemic lupus erythematosus, rheumatoid arthritis, poststreptococcal glomerulonephritis, IgA nephropathy, serum sickness, hypersensitivity pneumonitis (e.g., farmer’s lung) |
|IV (Delayed) ||2 to 3 days ||Contact dermatitis, poison oak/ivy, tuberculin skin test reaction, drug rash, Stevens-Johnson ...|