Abstract
Animal models and clinical studies of asthma have generated important insights into the first effector phase leading to the development of allergic airway disease and bronchial hyper-reactivity. In contrast, mechanisms related to asthma chronicity or persistence are less well understood. The CD4+ T-helper 2 lymphocytes are known initiators of the inflammatory response associated with asthma. There is now increasing evidence that memory T-cells, sensitized against allergenic, occupational or viral antigens, are also involved in the persistence of asthma. Additionally, the role of pathogens in asthma has been linked to both the initial susceptibility to and flares of this disease. This review will discuss the potential links between infection and asthma, the role of the memory T-cells in asthma, and the potential mechanisms by which these factors interact to lead to the development and/or persistence of asthma.