Diesel exhaust particles and the airway epithelial cell-dendritic cell interface in the control of immune homeostasis

Traffic related air pollution is associated with sensitization to inhaled allergens. Airway epithelial cells are the first targets of airborne pollutants and synthesize and release chemokines and cytokines implicated in local immune responses. Dendritic cells (DC) are abundant in the subepithelial mucosa and rapidly traffic to regional lymph nodes. DC regulate the multiplicity of T cell effector responses that result in the initiation and maintenance of airway inflammation. DC also regulate the less well understood regulatory T cell responses, including the generation of "adaptive" or peripheral T regulatory cells, that result in tolerance to antigens. This chapter will focus on the epithelial cell-dendritic cell interface in the control of effector and regulatory T cell homeostasis of the airway and the disruption of homeostasis by ambient pollutants. The ability of ambient pollutants, specifically diesel exhaust particles (DEP), to modify epithelial cell-derived signals, including CCL20, granulocyte macrophage-colony stimulating factor (CSF2), and thymic stromal lymphopoeitin (TSLP) for recruitment of DC subsets, DC maturation and DC polarization are described.