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A principal biological role of the immune system is an eradication of both external as well internal violators of integrity of the organism. External „enemies“ are represented mainly by germs; those of internal origin belong especially to potentially malignant cells that appear in our organisms as the results of a breakdown of their replication mechanisms.Under certain circumstances, however, the immune response can have deleterious effects, resulting in significant tissue damage or even death. This inappropriate immune response is termed hypersensitivity. Although the word hypersensitivity implies an increased response, the response is not always heightened but may, instead, be an inappropriate immune response to an antigen.
Several forms of hypersensitive reaction can be distinguished, reflecting differences in the effector molecules generated in the course of the reaction. In immediate hypersensitive reactions different antibody isotypes induce different immune effector molecules. IgE antibodies, for example, induce mast cell degranulation with release of histamine and other biologically active molecules. IgG and IgM antibodies, on the other hand, induce hypersensitive reactions by activating complement. The effector molecules in these reactions are the membrane-attack complex and such complement split products as C3a, C4a and C5a. In delayed-type hypersensitivity reactions, the effector molecules are various cytokines secreted by T helper cells and macrophages. As it became clear that different immune mechanisms can give rise to hypersensitive reactions, P. G. H. Gell and R. R. A. Coombs proposed a classification scheme in which hypersensitive reactions are divided into four types, I, II, III, and IV, each involving distinct mechanisms; later type V was added. Antibodies mediate four types of hypersensitive reactions: IgE-mediated (type I), cytotoxic (type II), immune complex (type III), and stimulatory/inhibitory (type V) hypersensitivity, respectively. T cells initiate the last type of hypersensitivity (type IV) and clinical symptoms appear more days after exposure; it is therefore referred to as delayed-type hypersensitivity (DTH). However, a great deal of com¬plexity exists within each type of reactions that blurs the boundaries between them.
 

Type I hypersensitivity belongs to the most common disorder mediated by immune reactions; it affects app. more than 30% of all individuals in Caucasoid population. Type I hypersensitivity is commonly called allergy. It is characterised by rapid onset (hence the term immediate hypersensitivity), within minutes of antigen challenge, and results in conspicuous clinical symptoms.