ABSTRACT

I. INTRODUCTION Immunoglobulin E (IgE), a key player in allergic inflammatory processes in allergic rhinitis, asthma, anaphylaxis, allergic gastroenteritis, and perhaps atopic dermatitis, is one of five immunoglobulin classes making up the humoral immune system. The IgE immune system, very recent in phylogenetic development, is found only in mammals (1). Though originally intended to ward off parasites, it has proved to be a double-edged sword, with harmful effects imparted on the host as well. Binding of multivalent antigens to IgE antibodies on their cell membranes initiates a chain reaction that releases pro-inflammatory mediators and cytokines from mast cells and basophils. There is strong organ specificity in this response due to homing of mast cells to mucosal tissues exposed to the external environment, local synthesis of IgE, upregulation of the receptor FCtRI on mast cells by IgE, consequent downregulation of FcyR, and slow dissociation of IgE from FCtRI.

Though the concentration of IgE is very low in the circulation, local synthesis of IgE easily compensates for the loss of IgE from the surface of mast cells, resulting in a prolonged inflammatory potential. This chapter provides an overview of the basic immunobiology of IgE and specific cells that participate in pathophysiologic mechanisms of the allergic response.