Antibodies are divided into different classes and subclasses (isotypes) according to structural differences in the constant region of the heavy polypeptide chains. The different isotypes mediate specific biologic functions that are important for the response to pathogens and in the pathogenesis of immunological diseases such as allergies. The numbers of different isotypes vary in different species, humans have 9 different Ig classes and subclasses. Of these 9, only IgM, IgG1, IgG2 and IgG3 activate the classical pathway of complement. All four IgG and both IgA subclasses, but not IgM, IgE and IgD, bind to Fc receptors on neutrophils, and induce the release of granule enzymes. All four IgG subclasses but no other Ig isotype induce serotonin release from platelets. In man, only IgE binds to the high-affinity Fc receptors (FcεRI) on mast cells and basophils and induces histamine and leukotriene release. IgE also binds to low-affinity Fc receptors (FcεRII) on lymphocytes, monocytes and eosinophils; however, the functions of FcεRII on these cells are not fully established. Monocytes from patients with atopic dermatitis that express more FcεRII than monocytes from normals do not release more LTC4 than monocytes from nonallergic healthy humans after activation with aggregated IgE. IgG and IgA are more efficient than IgE in inducing the release of mediators of inflammation from monocytes. The antibody response to certain antigens such as carbohydrates and allergens are often restricted to IgG2 and IgG1, IgG4 and IgE, respectively. Although the control of the Ig class expression is not understood, it was recently shown that interleukin-4 (IL-4) secreted by T helper cells plays a major role in the human IgM to IgG4 and IgE switch mechanism, both isotypes being characteristics for antibodies to allergens. However, the reason why allergens activate predominantly T helper cells secreting IL-4 is unknown. It may be because allergens are processed by special antigen-presenting cells that cause T helper cells to differentiate into IL-4-secreting cells.

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