abstract
- Under normal circumstances the lung is in a state of immunologic homeostasis, a condition in which exposure to innocuous antigens does not lead to immune-inflammatory responses. This is the only reasonable solution to the dilemma faced by the lung: The need to interact with the external environment and the need to avoid responding to most of the environmental antigens to which it is exposed. In allergic diseases, such as asthma, this homeostasis is undermined, and immuneinflammatory responses to harmless aeroallergens are activated. We describe the changes in antigen presentation and cellular activation observed in a model of allergic airway inflammation. Further, we present a summary of our work that investigated the impact of the airway cytokine microenvironment on the development of immune responses in the respiratory tract.