Atopic allergic individuals are prone to develop one or more atopic diseases such as allergic rhinitis (AR), allergic kerato-conjunctivitis, allergic asthma or atopic dermatitis (AD). Under normal circumstances, innocuous proteins delivered through the outer surfaces into regional lymph nodes do not evoke strong immune reactions but induce antigen-specific hypo responsiveness. The cellular mechanisms that develop after allergen encounter are understood only very incompletely, and the contributions of the various types of cells involved in T cell hypo responsiveness toward allergens are insufficiently defined. In patients with atopic disorders, periods of disease aggravation alternate with phases of remission, even in the presence of the offending allergen(s). A complex interrelation of genetic, environmental, psychological, and immunological factors may account for the manifestation of allergic inflammation [1, 2]. Atopic individuals show an inherited dominance of T H2 responses. Blood T cells of these patients respond to allergens such as birch pollen allergen, with the production of Interleukin (IL)-4, IL-5, and IL-13 rather than Interferon (IFN)-γ (which is secreted by T H1 cells) as in healthy individuals. IL-4 and IL-13 are the principal mediators of the B cell antibody class, switching towards IgE and therefore are key initiators of IgE-dependent reactions. Interleukin-5 acts mainly on eosinophils as an activating cytokine. These different mediators produced by the same T cell subset account for the frequently observed high serum levels of IgE and activated eosinophils seen in TH2-dominated diseases. In AD, the initial TH2-cytokine-dominated acute phase switches into a second phase, this is predominated by TH1 cytokines such as IFN-γ, leading to chronic skin lesions .
|Title of host publication||Natural Killer Cells: At the Forefront of Modern Immunology|
|Number of pages||12|
|Publisher||Springer Berlin Heidelberg|
|Publication status||Published - 2010|