Biological functions of IgE

The biological function(s) of IgE in cellular immunity can be related to its partnership with the high-affinity receptor, FceRI, on mast cells and Langerhans cells. Its interactions with the same receptor on eosinophils and monocytes are undoubtedly important also, but their significance is still somewhat obscure. Langerhans cells are bound in the epithelium and are thus favorably placed for the capture and processing of antigens recognized by IgE antibodies bound to FceRI. Following antigen capture the cells travel through the circulation to lymphoid tissues, where they stimulate T cells with specific receptors. Mast cells are distributed throughout the mucosa of tissues lining the skin, lungs and gut (major organs affected by allergic disease). When multivalent antigens bind to IgE antibody-sensitized mast cells and crosslink the receptors, several processes ensue: 1) the cell degranulates, causing release within minutes of histamine and other stored mediators of inflammation, including the potent cytokines, IL-4 and tumor necrosis factor a (TNFa); 2) lipid mediators are synthesized and released (also within minutes); and 3) several genes encoding inflammatory cytokines, including IL-4, IL-5, IL-6, IL-13, granulocyte-macrophage colony-stimulating factor and TNFa are activated (over a period of many hours). The local high concentrations of the mediators and cytokines leads to: 1) vasodilatation; 2) increased capillary permeability, causing the leakage of macromolecules and cells into the tissues (which results in the edema, referred to above); 3) airway smooth muscle contraction (which impedes entry of further airborne antigens to the lungs) and bowel movement (to expel parasites); and 4) upregulation of adhesion molecules (e.g. ELAM, VCAM-1 and ICAM-1) on endothelial cells lining the tissues, which results in the recruitment of inflammatory cells (notably, T cells, eosinophils and macrophages). These conditions initiate a 'leukocyte cascade' or inflammatory response, centering on the sites of antigen provocation. The allergic response is divided into two phases, an 'immediate' response, termed 'type I hypersensitivity' in the medical literature, and the 'late phase response', or subsequent inflammatory reaction.

It has long been thought that localised anaphylaxis evolved in mammals to enable them to eliminate parasites, but that it has become largely deleterious in humans, since, at least in allergic individuals, it is triggered by innocuous substances and is then manifested as allergy. It must be kept in mind, however, that parasites such as Schistosoma mansoni are endemic in many parts of the world and epidemiological (if not experimental) evidence suggests that IgE is protective. It is also possible that this response, essentially unique to the IgE antibody class, has as yet undiscovered functions.

On the whole, allergy is a concern in the more highly industrialized parts of the world, where immunology is mainly practised and where intensive efforts are being made to understand the 'pathogenesis' of allergy. Allergic conditions include hayfever or rhinitis (the most common), asthma, atopic dermatitis, food allergy and allergic uveitis (affecting the eyes). Anaphylactic shock is the only manifestation of the response that is systemic in nature, and thus differs from the others, which predominantly affect single organs. There has been an alarming increase, corresponding to a 10-year doubling rate, in the incidence of allergic disease in the industrialized parts of the world over the last few decades. Now one in five adults suffers from some form of allergy and a similar proportion of children suffer from asthma. IgE is implicated in the pathogenesis of allergy, as a key component in both the afferent (by way of dendritic cells and B cells) and the efferent (by way of mast cells and basophils) limbs of the immune response. The reasons why some individuals, but not others, are predisposed to this outcome are not well understood.

See also: Allergens; Atopic allergy; Basophils; Mast cells; B lymphocytes; CD40 and its ligand; Fc receptors; Immunoglobulin structure; (nterleukin 4.

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