TY - JOUR
T1 - PAMPs and DAMPs
T2 - Signal 0s that spur autophagy and immunity
AU - Tang, Daolin
AU - Kang, Rui
AU - Coyne, Carolyn B.
AU - Zeh, Herbert J.
AU - Lotze, Michael T.
PY - 2012/9
Y1 - 2012/9
N2 - Summary: Pathogen-associated molecular pattern molecules (PAMPs) are derived from microorganisms and recognized by pattern recognition receptor (PRR)-bearing cells of the innate immune system as well as many epithelial cells. In contrast, damage-associated molecular pattern molecules (DAMPs) are cell-derived and initiate and perpetuate immunity in response to trauma, ischemia, and tissue damage, either in the absence or presence of pathogenic infection. Most PAMPs and DAMPs serve as so-called 'Signal 0s' that bind specific receptors [Toll-like receptors, NOD-like receptors, RIG-I-like receptors, AIM2-like receptors, and the receptor for advanced glycation end products (RAGE)] to promote autophagy. Autophagy, a conserved lysosomal degradation pathway, is a cell survival mechanism invoked in response to environmental and cellular stress. Autophagy is inferred to have been present in the last common eukaryotic ancestor and only to have been lost by some obligatory intracellular parasites. As such, autophagy represents a unifying biology, subserving survival and the earliest host defense strategies, predating apoptosis, within eukaryotes. Here, we review recent advances in our understanding of autophagic molecular mechanisms and functions in emergent immunity.
AB - Summary: Pathogen-associated molecular pattern molecules (PAMPs) are derived from microorganisms and recognized by pattern recognition receptor (PRR)-bearing cells of the innate immune system as well as many epithelial cells. In contrast, damage-associated molecular pattern molecules (DAMPs) are cell-derived and initiate and perpetuate immunity in response to trauma, ischemia, and tissue damage, either in the absence or presence of pathogenic infection. Most PAMPs and DAMPs serve as so-called 'Signal 0s' that bind specific receptors [Toll-like receptors, NOD-like receptors, RIG-I-like receptors, AIM2-like receptors, and the receptor for advanced glycation end products (RAGE)] to promote autophagy. Autophagy, a conserved lysosomal degradation pathway, is a cell survival mechanism invoked in response to environmental and cellular stress. Autophagy is inferred to have been present in the last common eukaryotic ancestor and only to have been lost by some obligatory intracellular parasites. As such, autophagy represents a unifying biology, subserving survival and the earliest host defense strategies, predating apoptosis, within eukaryotes. Here, we review recent advances in our understanding of autophagic molecular mechanisms and functions in emergent immunity.
KW - Apoptosis
KW - Autophagy
KW - DAMPs
KW - Immunity
KW - Inflammation
KW - PAMPs
UR - http://www.scopus.com/inward/record.url?scp=84865299726&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84865299726&partnerID=8YFLogxK
U2 - 10.1111/j.1600-065X.2012.01146.x
DO - 10.1111/j.1600-065X.2012.01146.x
M3 - Article
C2 - 22889221
AN - SCOPUS:84865299726
SN - 0105-2896
VL - 249
SP - 158
EP - 175
JO - Immunological Reviews
JF - Immunological Reviews
IS - 1
ER -