Hypersensitivity Antigen-antibody complexes

Type III hypersensitivity is due to the presence of elevated levels of antigen-antibody complexes that deposit on basement membranes in tissues and vessels. Immune complex deposition activates complement to produce components with anaphylatoxic and chemotactic activities (C5a, C3a, C4a) that increase vascular permeability and recruit neutrophils to the site of complex deposition. Complex deposition and the action of lytic enzymes released by neutrophils can cause skin rashes, glomerulonephritis, and arthritis in these individuals. If patients have type III hypersensitivity against a particular antigen, clinical symptoms usually occur 3-4 days after exposure to the antigen. 

Type II hypersensitivity results from the formation of antigen-antibody complexes between foreign antigen and IgM or IgG immunoglobulins. One example of this type of hypersensitivity is a blood transfusion reaction that can occur if blood is not cross-matched properly. Preformed antibodies bind to red blood cell membrane antigens that activate the complement cascade, generating a membrane attack complex that destroys the transfused red blood cells. In hemolytic disease of the newborn, anti-Rh IgG antibodies produced by an Rh-negative mother cross the placenta, bind to red... 

Trimellitic anhydride, used in chemical synthesis. Type II hypersensitivity manifested by adverse effects on blood, including hemolytic anemia and bone marrow depression, may be caused by exposure to trimellitic anhydride. This agent may also cause type III hypersensitivity, resulting from deposition of antigen-antibody complexes in tissue and causing symptoms such as rheumatoid disease or pneumonitis. 

Illustrated in Figure 3 is a likely over-all mechanistic role of theophylline in asthma. Extrinsic or immediate hypersensitivity-type asthma begins with an antigen -antibody complex at mast cells and results in the release of chemical mediators which affect cells in airways. Smooth muscle cells contract, capillaries leak, and secretory cells hypersecrete to give a triad of bronchospasm, edema and Increased mucous, respectively. Shown is the two-enzyme... 

Because these phenomena are also observed in other acute pulmonary reactions caused by antigen-antibody complexes, it is supposed that nitrofurantoin acts similarly, although Goldstein and Janicki (1974) had no success in demonstrating the specific antibody. In contrast, Pearsell et al. (1974) assume that pathogenesis is based on hypersensitivity of the prolonged type (cell-bound immune response). 

B cells Form plasma cells that secrete immunoglobulins (IgG, IgA, and IgE) Participate in antigen-antibody complex-mediated tissue damage (type III hypersensitivity)... 

Not all antigen-antibody reactions are of benefit to the body, as sometimes the complexes (or their subsequent interaction with body tissues) may result in tissue damage. This must be regarded as a malfunction of the immune system and is known as a hypersensitive reaction. These reactions can be categorized into five main types. The first three involve the interaction between antigen and humoral antibody, and as the onset of the reaction is rapid, the condition is termed immediate hypersensitivity. The fourth type (delayed hypersensitivity) involves T cells and the symptoms of the reaction appear after 24 hours. The fifth type is where antibody stimulates cell function. 

Immune Complex Disorder A disorder caused by anti-gen-antibody complexes that precipitate in the blood and injure tissues elicited by antigens in vaccines, on microorganisms, or on a person s own cells. Known also as Immune Complex (Type III) Hypersensitivity. 

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