ABSTRACT
T-lymphocytes play a major role in recognizing foreign antigens and orchestrating the immunological response. Activated T-lymphocytes apoptosis is essential for maintaining immune system homeostasis, and failure to clear activated cells prolongs the immune response and promotes chronic infl ammation. Experimental evidence suggests that apoptosis control mechanisms may be impaired in many infl ammatory conditions, particularly Th 2-type airway allergic diseases. Asthma is characterized by chronic infl ammation of airways and by structural alterations of bronchial tissues, oft en referred to as airway remodelling. Increased cellular recruitment and activation, enhanced cell survival and cross talk between T-lymphocytes and tissue microenvironment have a crucial role in the development of airway infl ammation, tissue damage, repair and remodelling in asthma. Research on animal models and humans focused mostly on T-cell-derived IL-4, IL-5 and IL13 as leading causes of airway infl ammation. New ‘biological’ anti-asthma agents which block specifi c pathways did not demonstrate impressive clinical eff ectiveness
on bronchial hyperreactivity, although they suppress eosinophil lung infi ltration. Drug, such as corticosteroids or cysteinyl-leukotriene receptor antagonists, which are directed at inducing T-lymphocyte apoptosis, seem to be associated with better clinical outcomes. Future studies should clarify how and when we can modulate these processes, perhaps combining and/or sequencing new biological and old anti-infl ammatory drugs.
