The Th1/Th2 paradigm in allergic asthma

The incidence of allergic asthma, which is characterized by chronic airway inflammation and airway hyperreactivity, has increased dramatically in the last two decades and is present in as many as 10% of individuals in industrialized nations. Allergic asthma is caused by an inappropriate immune response to common aero-allergens in genetically predisposed individuals. The central role in this immune response is played by CD4(+)T helper(Th)2 cells. Through the release of cytokines like interleukin (IL)-4, IL-13,and IL-5, Th2 cells orchestrate the recruitment and activation of mast cells, eosinophils and basophils and induce the production of IgE by B cells. While Th2 cells promote airway inflammation in asthma, interferon (IFN)-gamma producing Th1 cells are proposed to protect against allergic disease by dampening the activity of Th2 effector cells. Accordingly, new therapeutic strategies aim at inhibition of Th2 cells and promotion of Th1 cells. Recent studies demonstrated that Th1 cells are not always able to inhibit Th2 cell-mediated disease and can even be unexpectedly harmful. These studies indicate that the Th1/Th2 paradigm is more complex than initially appreciated and that suppression of allergic inflammation and Th2 activity may depend - at least in part - on cells other than Th1 lymphocytes.