Pathogens have long been known to cause both local and systemic inflammation via activation of the immune system. Classically, descriptions of immune regulation arose from the idea that immune cells can discriminate self from non-self, and activate innate immunity when there is foreign invasion. This model, which stemmed from work done in the 1960s by Burnet and Medawar, has been modified through the years to account for new discoveries in immune cell function (1, 2) . Although the self/nonself model is suitable in explaining immune activation and inflammation that occurs as a consequence of clinical scenarios, such as invasion by foreign pathogens or transplant rejection, it fails to account for the inflammation which occurs in settings such as trauma or autoimmunity, which are void of non-self stimuli. In an attempt to better describe these phenomena, Matzinger has proposed the concept of danger signaling (3) . In this model, initiation of the inflammatory response occurs in response to molecular patterns that are associated with both pathogens and some normal cellular components that are released by damaged cells during both infectious and sterile processes (4) . The concept of cellular communication by "danger signals," whether exogenous or endogenous, reconciled the paradox of immune activation in both infection and sterile injury.