The effectors of innate immunity: DAMPs, DAMEs, or DIMEs?

‘A rose by any other name would smell as sweet’ is one of the most famous lines in all of literature. The implication of this observation, spoken by Juliet about the troubles in Verona because Romeo was called Montague and Juliet Capulet, is that names do not matter; rather, it is the thing itself that is important. Of course, Shakespeare’s great line works because everyone knows what a rose is and that it smells sweet. What happens when the essence of a thing is not known and the name really matters? I think that such a situation is occurring right now in the field of innate immunity since the essence of many things is not fully known. As research progresses rapidly, new cells, molecules, and pathways are discovered and receive names, often an acronym or an abbreviation or sometimes a brand new coinage. Dendritic cells, Toll receptor, and inflammasomes are all of recent origin. The derivation of such words is often fascinating. After all, ‘toll’ comes from the German word meaning ‘great’ and became famous when a researcher working on Drosophila excitedly exclaimed ‘Das ist ja toll’ (‘That’s great’) when a critical immune defense system was discovered. To immunologists, toll now signifies a pattern recognition receptor (PRR). One area in which nomenclature appears especially uncertain, ambiguous, and even controversial concerns the proper designation for molecules that are released from dead, damaged, and stressed cells to serve an immunological function in the extracellular space. These molecules have received various names, including danger molecules, alarmins, hyppos, and DAMPs. The current favorite seems to be DAMP, which stands for death (or danger or damage)-associated molecular pattern. An appealing feature of the word DAMP is the analogy with PAMP, or pathogen-associated molecular pattern.