Responses to Antibody Binding

Allergic urticaria. Histamine and other pro-inflammatory substances are released from mast cells in the skin and tissues in response to the binding of allergen-bound IgE antibodies to high-affinity cell-surface receptors. Basophils and other inflammatory cells release histamine and other mediators, and are thought to play an important role, especially in chronic urticarial diseases. 

Haptens, a special class of antigen, are small molecules that induce specific antibody production when they are attached to a protein that acts as a carrier. Phosphorylcholine is one such hapten that has been widely used in the investigation of immune responses. The specific binding of this hapten... 

Type I allergic reactions are inappropriate immune responses to an allergen with preferential synthesis of immunoglobulin E (IgE), a special antibody class, which binds to mast cells and basophilic granulocytes via Fee receptors. Binding of the allergen to the cell-bound IgE initiates the rapid release of allergic mediators, most prominently histamine, and the de novo synthesis of arachidonic acid metabolites and cytokines, which are responsible for the clinical symptoms. 

Fig. 9. Representation of the use of the modification of an ionophore s potentiometric response in order to detect antibody binding. A constant ion activity (in this case K ) must be maintained in the sample solution...

Type II reactions are produced by IgG (or IgM) antibody. The drug or hapten that elicited the antibody response binds to target cells. When antibody binds the drug, complement activation destroys the cell. Blood dyscrasias such as thrombocytopenia and hemolytic anemia are the most common examples of type II reactions. 

Factor VIII and IX inhibitors are antibodies that develop in 20% and 12% of hemophilia A and hemophilia B patients, respectively, in response to replacement therapy. These antibodies bind to and neutralize the activity of infused factor concentrates. Although the inhibitors do not increase hemorrhage frequency, their existence challenges the treatment of bleeding episodes. Titers of inhibitors are measured and... 

Xu et al. [5] described the effect of (z>)-penicillamine on the binding of several antiacetylcholine receptor monoclonal antibodies to the Torpedo acetylcholine receptor. Penicillamine is covalently incorporated into the acetylcholine receptor through SS exchange at the cysteine residues of the a-subunit, altering the antigenic structure of the receptor. This effect on the structure of the native receptor at the neuromuscular junction may be responsible for the establishment of the autoimmune response to the acetylcholine receptor in (i))-penicillamine-induced myasthenia gravis. Cysteine and penicillamine interact to form penicillamine-cysteine mixed disulfide complexes [6] ... 

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