RESUMO
IgE antibodies, when cross-linked by allergen on the surface of effector cells such as mast cells and basophils, are known to be directly responsible for immediate type hypersensitivity reactions. In addition, IgE may be involved in other, indirect, mechanisms, fundamental to the pathogenesis of allergic diseases, such as enhancement of the antigen capturing capacity of antigen presenting cells. IgE mediated antigen presentation could lead to a continuous activation of the immune system by very low concentrations of allergen. As a result, Th2 cell populations may expand and may induce more B cells to switch to IgE production. Subsequently, the overproduction of IgE and Th2 cells in a patient may explain the clinical observation that certain allergic patients deteriorate from sensitivity to a single group of allergens to sensitivity to multiple groups of allergens. Therefore, control of IgE production is not only important for the treatment of allergic symptoms, but may also regulate deterioration of allergy via the mechanism of CD23/IgE mediated allergen presentation by naive B cells. The role that monocytes, which have recently been found to express Fc epsilon RI, play in the pathogenesis of allergy, remains speculative. We hypothesize that their role may be to remove IgE from the circulation and re-direct the immune response from naive B cells. IgG antibodies which cannot be used for antigen uptake by B cells also direct the immune response to monocytes.
