V o l . 2 0 N o . 7 3 1 7 llergic responses to common environmental antigens, such as those derived from house dust mites, plant pollens or animal proteins, lead to clinical disorders such as asthma, hay fever, eczema and allergic rhinitis. The reasons why only some individuals develop these atopic disorders are poorly understood. The current view is that genetic and environmental factors interact with each other, leading to the production of interleukin 4 (IL-4) through Stat6-mediated signalling and the activation of specific downstream transcription factors such as c-Maf, GATA3, NIP45 and NFATc in naive T cells, resulting in the development of allergen-specific T helper 2 (Th2) CD4 Ο© T cells. Once generated, Th2 cells activated by allergen secrete IL-4 and IL-5, cytokines that induce the production of IgE and IgG1 by B cells, as well as stimulating the development of eosinophils in the bone marrow and their recruitment into inflamed tissues 1Γ6 .
It is believed that the most important factor governing the pathogenesis of atopic disorders is the crosslinking of IgE Fcβ receptors on mast cells, after encountering allergen, which leads to mast cell degranulation. The molecules released by mast cells include histamine, heparin and proteases, which mediate biological effects including vasodilatation, intestinal and/or bronchial smooth muscle contraction, mucous secretion and local proteolysis. After the initial immediate reaction of the mast cells, an influx of eosinophils, basophils and lymphocytes occurs, 6Γ24 h later. This late-phase response can lead to chronic inflammation of tissues continuously exposed to antigen. This course of events is especially evident in asthmatic disease, where chronic swelling and inflammation of the airways can lead to a sudden and violent constriction upon allergen challenge 1,2 . What follows will be a discussion of how some infectious diseases may influence both the development of allergic disorders and their effector mechanisms.