Effect of Immunotherapy on Humoral and Cellular Markers in Allergic Patients

Abstract

The main feature of allergic disease is an IgE-mediated inflammation, while an essential feature of both allergic and nonallergic asthma is bronchial hyperresponsiveness (BHR). The term “bronchial hyperresponsiveness” generally refers to an increase in airway sensitivity against a number of pharmacological, physical and chemical stimuli. The different stimuli induce BHR through different pathways which may represent a variety of pathophysiological conditions. At least in allergic asthma the degree of nonspecific responsiveness to commonly used stimuli like histamine or methacholine seems to represent variable degrees of inflammation. Although many different cells play a role in this inflammatory process, the eosinophil granulocyte dominates the picture. A selective increase in the number of activated eosinophils has been found in circulating cells of peripheral blood, and also in BAL (bronchoalveolar lavage) fluid and biopsies from mucosa of allergic and nonallergic asthmatics. Another cell type of central importance for the inflammatory process in allergic asthmatic disease is the lymphocyte. T lymphocytes produce a number of cytokines with different properties, covering a large span of activities such as the effect on hematopoietic cells, leading to differentiation and maturation of cells central to the allergic process, mast cells and eosinophils. Another important activity is the helper function in production of IgE antibodies from B cells. The Th2 cell type orchestrates these processes by production of a selective array of cytokines: interleukin-3 (IL-3), IL-4, IL-5 and granulocyte/ macrophage-colony-stimulating factor (GM-CSF). This new understanding of the inflammatory process was possible due to the development of immunohistochemical and molecular techniques which have been applied to the biological material taken from patients affected with allergic disease.