Immune parameters in high-risk atopic individuals during early childhood.

The profile of cytokine production by peripheral blood mononuclear cells (PBMCs) from patients with bronchial asthma on stimulation with house dust mite was demonstrated to be compatible with that of helper T type 2 (Th2) cells (1). The number of Th2 cells was also shown to be increased in bronchial tissue and bronchoalveolar lavage fluid of patients with bronchial asthma. Also, the recruitment of allergen-specific Th2 cells from the peripheral blood into the bronchial tissue after an inhalant allergen challenge was demonstrated. Allergic asthma is therefore considered a Th2-driven disease in which the presence of Th2 cells correlates with IgE production, mast cell hyperplasia, and eosinophil infiltration, determining the severity of the disease (2). The Th2-derived cytokine interleukin 5 (IL-5) is a crucial cytokine, which accounts for the recruitment and activation of eosinophils, resulting in airway eosinophilia in patients with allergy (3). In animal models, depletion of CD4 1 T cells results in abrogation of airway eosinophilia and in subsequent reduction of airway hyperresponsiveness. Similarly, elevated IL-4-induced serum levels of IgE and allergen-specific IgE levels as observed in patients with atopic allergy can be explained in terms of excessive Th2 activation. Many, but not all, the pleiotropic effects of IL-4, which are of importance in allergic diseases, can be inhibited by interferon g (IFNg ). Thus, the balance between Th1/Th2 activation is generally established by determining the ratio between IL-4 and IFNg produced by activated PBMCs or purified T cells.