Cytokines in allergic inflammation

Abstract

In the recent years our knowledge about the pathogenesis of allergic diseases has increased considerably. This progress is due to a large degree to rapid developments in fields which at first sight are not directly related to allergy such as cellular immunology, molecular biology and inflammation research. There is now a general consent that asthma and allergic rhinitis are inflammatory pathologies and that the extent of the inflammatory response determines by large the severity of allergic disease. This concept has already led to clear changes in the therapeutical management of allergic diseases in that anti inflammatory therapy is used as a first-line treatment while short acting bronchodilators are rather used to relieve the remaining symptoms on a “on demand” basis. However, an inflammatory response is a rather stereotypical albeit very complex reaction of the macroorganism to tissue damage of different causes. In general, inflammatory reactions start with a vascular phase (plasma exudation / edema) followed by infiltration of the tissue by leukocytes (cellular exudate/tumor) and finally tissue repair, remodeling or fibrosis. The cellular phase of inflammation leads itself to tissue damage by activation of infiltrating effector cells and release of secondary inflammatory mediators and cytotoxic products (basic proteins, proteases, oxygen radicals etc.). Inflammatory reactions of different etiologies probably display more common features than dissimilarities, and all leukocyte types — and even platelets and tissue cells — participate to various degrees in a complex network of cellular interactions. These cellular interactions and effector functions are controlled by a very large number of mediators and cytokines. IgE-mediated allergic reactions are classically divided into an immediate response involving edema and smooth muscle contraction due to the release of mediators by mast cells and the late phase reaction characterized by cellular infiltration and tissue damage, although, in clinical practice, the continuous exposure to allergens results in a chronic inflammatory process.