In our research projects, we are trying to understand what mechanisms are employed by our innate immune system to distinguish self from non-self. Central to this complex task is a repertoire of pattern recognition receptors (PRRs) that have evolved to detect the presence of microorganisms. The ligands or targets of these PRRs are usually referred to as pathogen-associated molecular patterns (PAMPs). PAMPs are typically molecular structures that are unique to the physiological processes of microorganisms but not the host. In addition, PAMPs usually constitute products that are essential to microorganisms and thus cannot be changed or lost by the respective microorganism via adaptive evolution. In addition to the recognition of PAMPs, some PRRs can also detect endogenous danger and stress situations. Cell stress or tissue damage can lead to the release of normally compartmentalized molecules or the chemical modification of self-molecules. These and other endogenous inflammatory signals that appear after cellular damage or due to metabolic derangements are collectively known as danger-associated molecular patterns (DAMPs), and their ability to trigger inflammation is mediated by the PRRs of our innate immune system.