The Role of NOD-Mediated Innate Immune Activation in

The ability to recognize and remove pathogens that invade the lower airway, while maintaining homeostasis in the lung microenvironment, is an essential function of the innate immune system. An evolving hypothesis in this relatively new area of research is that in addition to maintaining normal host function, the molecular machinery responsible for pathogen recognition and activation of the innate immune response, may also contribute to chronic inflammatory diseases if a break down in normal function occurs [9]. This thesis focuses on the investigation of NOD-like receptor proteins (NLRs) which are involved in intracellular pathogen recognition and activation of the innate immune response. Recent work by others has identified that NOD1 and NOD2, of the NLR family, are critical components in intestinal inflammatory diseases [1]. An association between NOD1 and NOD2 with autoimmune diseases of the lung, primarily asthma and sarcoidosis respectively, has also been described [3,11]. The main goal of this thesis i