Interaction of surfactant with airway inflammation in asthma. After uptake through the airway surfactant barrier (right side of figure), allergens are presented by dendritic cells (DC) to T cells (T) that release IL-2, proliferate, and differentiate into T helper 2 lymphocytes (Th2). These Th2 cells release cytokines (IL-4 and IL-5) that attract eosinophils (Eos) and stimulate IgE production by differentiated B lymphocytes (B). IgE is bound to mast cells (MC) that, upon stimulation with allergen, release mediators (such as histamine) inducing acute asthma attacks. Activated eosinophils degranulate and release toxic mediators like eosinophil cationic protein (ECP), leukotrienes (LT), and transforming growth factor-β (TGF-β) that induce epithelial damage and chronic airway inflammation. ECP is shown in bold because ECP, but not LT or TGF-β, has been shown to cause surfactant dysfunction (unpublished data). The various effects of surfactant proteins SP-A, SP-B, SP-C and SP-D are indicated. SP-A and SP-D are shown in bold to emphasize the importance of these surfactant molecules as immunomodulators in asthma. Mechanisms of stimulation, activation, induction, or release are symbolized by arrows whereas inhibition, decrease, or down-regulation are symbolized by lines terminated by =. ? is used to indicate that the effects of SP-A/SP-D are presently unclear. PL = phospholipid.