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Abstract
Immune responses are initiated and perpetuated by molecules derived from microorganisms
pathogen-associated molecular-pattern molecules or from the damage or death of host
cells [damage-associated molecular-pattern (DAMP) molecules]. Many DAMPs are nuclear
or cytosolic proteins with defined intracellular function that, when released outside
the cell following tissue injury, move from a reducing to an oxidizing milieu resulting
in their functional denaturation. Here, we discuss the consequences of DAMP oxidation
on the outcome of acute inflammation. We also suggest that, outside the cell, DAMPs
might adopt novel conformations or alter the redox of the extracellular environment
to more closely mimic the internal one, thereby avoiding oxidation-mediated inactivation
and promoting pathology. We propose that chronic inflammation associated with autoimmunity,
chronic viral infection and cancer is probably mediated by persistent release and
function of DAMPs, promoting and promoted by a disordered redox environment.