DAMPs are endogenous danger signals that are discharged to the extracellular space in response to damage to the cell from mechanical trauma or a pathogen.
[4] Inflammation is a key aspect of the innate immune response; it is used to help mitigate future damage to the organism by removing harmful invaders from the affected area and start the healing process.
Administration of recombinant human superoxide dismutase (rh-SOD) in recipients of cadaveric renal allografts demonstrated prolonged patient and graft survival with improvement in both acute and chronic rejection events.
[9] The second study[10] suggested the possibility that the immune system detected "danger", through a series of what is now called damage-associated molecular pattern molecules (DAMPs), working in concert with both positive and negative signals derived from other tissues.
Thus, these papers anticipated the modern sense of the role of DAMPs and redox, important, apparently, for both plant and animal resistance to pathogens and the response to cellular injury or damage.
[1] DAMPs vary greatly depending on the type of cell (epithelial or mesenchymal) and injured tissue, but they all share the common feature of stimulating an innate immune response within an organism.
The main role of DAMPs in plants is to act as mobile signals to initiate wounding responses and to promote damage repair.
The ETI always occurs after the PTI pathway and DAMP release, and is a last resort response to the pathogen or trauma that ultimately results in programmed cell death.
The PTI- and ETI-signaling pathways are used in conjunction with DAMPs to rapidly signal the rest of the plant to activate its innate immune response and fight off the invading pathogen or mediate the healing process from damage caused by trauma.
The blocking of DAMPs also has theoretical applications in therapeutics to treat disorders such as arthritis, cancer, ischemia reperfusion, myocardial infarction, and stroke.