The blood-gas barrier of the lung is topologically on the outside of the body and thus is at risk of attack from environmental insults. The lung has evolved elaborate defense mechanisms to deal with this threat, the final line of defense being the immune system. Models of immunity in the lung based on systems of ordinary differential equations can be used to explore the effectiveness of pharmaceutical therapies. Models based on systems of partial differential equations can be used to explore how viruses and bacteria affect the integrity of the pulmonary epithelial barrier. Agent-based models of the interactions between the cells of the immune system and the tissue on which they operate can recapitulate the transient nature of allergic inflammation in the lung. An agent-based model has been used to test the plausibility of the idea that allergic inflammation progresses with a predetermined time course much like a muscle twitch or a nerve action potential, albeit over a much longer duration. A corollary of this idea is that there should be a refractory period to the initiation of allergic inflammation, something for which there is experimental evidence. This suggests that such an “inflammatory twitch” might fail to resolve in asthma.