New perspectives in the modulation of allergic inflammation.

Studies on the regulation of IgE synthesis by IgE cellular receptors or fragments thereof, the so-called IgE-binding factors, are currently attracting much attention. Even more important may be some lymphokines such as interleukin 4 and interferon gamma which have been shown to have opposite influences on IgE synthesis, both in vitro and in vivo. However, the role of anti-isotypic anti-IgE antibodies, which have been shown to occur frequently during an IgE response, also deserves to be further investigated. At the effector level, namely the development of immediate and late allergic reactions following renewed encounter with allergen, new concepts such as variable releasability and priming of effector cells by lymphokines have opened new investigative pathways. Indeed, pretreatment of neutrophils by granulocyte/monocyte colony-stimulating factor or basophils by interleukin 3 appears essential for production or optimal release of inflammatory mediators such as histamine, leukotrienes, or platelet-activating factor. Even the successive impact of purified lymphokines such as interleukins 3 and 8 on basophils may suffice to initiate mediator release. These phenomena may explain, at the molecular level, the induction of a state of hyperreactivity characteristic of the late-phase allergic reaction. They also suggest new immunopharmacological approaches for the treatment of allergy.