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1 DAMP recognition by dendritic cells (DCs) has also been
2 DAMPs are recognized by the innate immune system via pat
3 DAMPs encompass a group of heterogenous molecules, inclu
4 DAMPs represent a heterogeneous group of molecules that
5 DAMPs trigger innate immunity by activating Toll-like re
6 DAMPs within the tumor microenvironment stimulate tumor-
7 observed that circulating levels of these 2 DAMPs are increased in hypertension, and activation of T
9 and blocked by atropine methylbromide and 4-DAMP mustard, an M(3) muscarinic receptor selective anta
11 elective muscarinic M3 receptor antagonist 4-DAMP (100 nmol/L) but was blocked by the M2 receptor ant
14 s inhibited by the m3 receptor antagonist, 4-DAMP, and binding to Galphai3 antibody was inhibited by
15 In contrast, the M3-selective antagonist, 4-DAMP-mustard, blocked muscarinic excitations in a majori
21 yperpolarization was reversibly blocked by 4-DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nit
23 ts, identifying both rapidly dissociating (4-DAMP, himbacine) and slowly dissociating (tiotropium, gl
24 (3) receptor pathway was blocked by either 4-DAMP or by intracellular dialysis with anti-Galphaq anti
25 -(2-chloroethyl)-piperidine hydrochloride (4-DAMP mustard; M3) were incubated with carbachol to deter
27 nylacetoxy-N-methyl-piperidine methiodide (4-DAMP) was 57-244-fold smaller than that of pirenzepine,
30 act cells, and the m3-mAChR selectivity of 4-DAMP and pFHHSiD was 2.4- and 3.9-fold less in membranes
33 order of potency (atropine > pirenzepine = 4-DAMP >> gallamine) consistent with regulation by M1, rat
37 coding double-stranded RNA (dsRNAs) act as a DAMP in the skin and how the human cathelicidin AMP LL-3
38 ypothesis that OGs released in vivo act as a DAMP signal to trigger plant immunity and suggest that c
44 uggest that under disease relevant acidosis, DAMPs and lactic acid induce the secretion of IL-1beta i
46 nose (PCAM), 1-deoxy-1-aminomannopyranoside (DAMP), glucosamine and low molecular weight chitosan bon
53 age-associated molecular patterns (PAMPs and DAMPs) orchestrate inflammatory responses to infection a
55 tanding that oxidation-specific epitopes are DAMPs, and thus the target of multiple arcs of innate im
56 ctors, as well as unsolved questions such as DAMP release from non-tumor cells as well as the existen
57 demonstrated that both S100A4 and UA act as DAMPs and, as such, may play a critical role in promotin
58 report that endogenous histones function as DAMPs after ischemic injury through the pattern recognit
59 esis that bone matrix components function as DAMPs for the NLRP3 inflammasome and regulate osteoclast
61 irect toward strategies aimed at attenuating DAMP-mediated inflammation while preserving antimicrobia
65 ve immune responses are triggered in vivo by DAMPs induced by tumor progression are not well characte
66 we will review the contribution of candidate DAMPs and their receptors, and discuss the evidence for
68 ytotoxic anticancer treatment, tumor-derived DAMPs (damage-associated molecular patterns) can be sens
71 that the production of HMGB1, an established DAMP released by dying cells, was critical for tumor pro
73 heir receptors, and discuss the evidence for DAMPs as tumor-promoting and anti-tumor effectors, as we
76 culture conditions, and it is not known how DAMPs signal under disease relevant conditions such as a
77 fecting activation, some recently identified DAMP receptors control specialised DC functions such as
79 initiated by the lipid-soluble azo initiator DAMP, dimethyl 2,2'-azobis (2-methylpropionate), while Q
81 Recent evidence has indicated that the major DAMP driving host antitumor immune responses is tumor-de
84 e we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally impo
85 disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bact
86 the hypothesis that acidic conditions modify DAMP-induced IL-1beta release from cultured primary mous
87 mage-associated molecular pattern molecules (DAMPs) are cell-derived and initiate and perpetuate immu
89 mage-associated molecular pattern molecules (DAMPs) such as S100 proteins and high-mobility group box
90 mage-Associated Molecular Pattern molecules (DAMPs) suggested that, at best, early application at a s
92 s who developed MODS also had elevated mtDNA DAMP levels compared with those who did not (32.57 +/- 0
94 with SIRS had significantly increased mtDNA DAMP levels in all 4 sequences examined (32.14 +/- 0.90
96 determine relationships between plasma mtDNA DAMP levels and the occurrence of systemic inflammatory
98 tion; however, the link between plasma mtDNA DAMPs and outcome in severely injured human subjects has
99 rst observational evidence that plasma mtDNA DAMPs is associated with the evolution of SIRS, MODS, an
100 ions in animal models demonstrate that mtDNA DAMPs contribute to organ dysfunction; however, the link
101 cute myeloid leukemia (AML) exposed multiple DAMPs, including calreticulin (CRT), heat-shock protein
102 ted extracellular release of the necroptotic DAMP, IL-33, and reduced Myd88-dependent inflammation.
104 eveal that histones represent a new class of DAMP molecules and serve as a crucial link between initi
105 ical data have established the importance of DAMPs, which signal through innate pattern recognition r
106 On the other hand, cell death and release of DAMPs may also trigger chronic inflammation and, thereby
107 IRGM regulates necroptosis and release of DAMPs to induce gastrointestinal inflammation, linking I
110 nce of suitable models, the relative role of DAMPs released because of necrosis or leukocyte activati
111 nate pattern recognition receptors (PRRs) or DAMP-specific receptors, in regulating the alloresponse
114 Here, we comprehensively review known PAMPs/DAMPs recognized by plants as well as the plant PRRs des
115 However, in contrast to other known PAMPs/DAMPs, cellobiose stimulates neither detectable reactive
117 totypic damage-associated molecular pattern (DAMP) molecule and has been implicated in several inflam
118 P) is a damage-associated molecular pattern (DAMP) molecule which stimulates proinflammatory cytokine
119 art via danger-associated molecular pattern (DAMP) molecules, such as high mobility group box 1 prote
122 nstream damage-associated molecular pattern (DAMP) pathway activation in vivo and in vitro and in pat
123 tion of damage-associated molecular pattern (DAMP) receptors and a cytosolic complex termed the infla
124 mediate damage-associated molecular pattern (DAMP) response including elevations in heat-shock protei
125 ts as a danger-associated molecular pattern (DAMP) that initiates helminth-induced type 2 immune resp
127 ng as a danger-associated molecular pattern (DAMP) that stimulates cytokine production in neighboring
128 ectious damage-associated molecular pattern (DAMP), heparan sulfate (HS),(1) aggravates graft-versus-
129 id is a damage-associated molecular pattern (DAMP), released from ischemic tissues and dying cells wh
130 and pathogen-associated molecular patterns (DAMP and PAMP, respectively) through pattern recognition
133 al DNA damage-associated molecular patterns (DAMPs) accumulate in the circulation after severe injury
134 ), and damage-associated molecular patterns (DAMPs) activate families of pattern recognition receptor
135 danger/damage associated molecular patterns (DAMPs) and a reduction in immunoinhibitory miRNA, which
136 ion of damage-associated molecular patterns (DAMPs) and a response that includes secretion of cytokin
138 abolic damage-associated molecular patterns (DAMPs) and discuss potential targets for therapeutic int
139 act as damage-associated molecular patterns (DAMPs) and interact with pattern recognition receptors t
144 hrough danger associated molecular patterns (DAMPs) as a response to an insult (systemic inflammatory
146 ing as damage-associated molecular patterns (DAMPs) for pattern recognition receptors (PRRs) may repr
147 L) are danger-associated molecular patterns (DAMPs) generated in response to infection that can preve
148 ase of damage-associated molecular patterns (DAMPs) is a characteristic feature of most advanced tumo
150 zed as damage-associated molecular patterns (DAMPs) or pattern-associated molecular patterns (PAMPs)
151 Ps) or damage-associated molecular patterns (DAMPs) recognized by plant PRRs induces both local and s
152 ing to damage-associated molecular patterns (DAMPs) released by injured host cells unleashes an infla
153 uch as damage-associated molecular patterns (DAMPs) released from injured cells to stimulate innate i
154 ogenic damage-associated molecular patterns (DAMPs) released into the circulation from football-induc
155 iverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, cerami
157 s) and danger-associated molecular patterns (DAMPs) to influence the activation and trafficking of DC
158 ensing damage associated molecular patterns (DAMPs) to sensing all particulate matter irrespective of
159 ept of damage-associated molecular patterns (DAMPs) was proposed to describe plant elicitors like oli
161 ase of damage-associated molecular patterns (DAMPs), and progressing through innate and adaptive immu
162 AMPs), danger-associated molecular patterns (DAMPs), and the more recent discovery of the role of the
163 ls, or damage-associated molecular patterns (DAMPs), are generated in response to cell stress and act
164 o host danger-associated molecular patterns (DAMPs), but not to microbial pathogen-associated molecul
166 termed damage-associated molecular patterns (DAMPs), have been proposed to activate dendritic cells (
167 to as danger associated molecular patterns (DAMPs), including those triggered by crystalline particu
168 MPs or damage-associated molecular patterns (DAMPs), such as uric acid or ATP, via NLRP3, which leads
169 er- or damage-associated molecular patterns (DAMPs), which are also perceived by PRRs to modulate PTI
185 s of 'danger associated molecular patterns' (DAMPs), against which a concerted innate immune response
186 ounds (damage-associated molecular patterns, DAMPs) such as peptides released from cells upon attack.
187 lled "damage-associated molecular patterns," DAMPs), as they die in the context of failing adaptive r
188 cells (damage-associated molecular patterns; DAMPs) activate cellular receptors leading to downstream
189 density-associated mutation-rate plasticity (DAMP) at multiple loci in both eukaryotes and bacteria,
191 ross-talk with various non-immune receptors, DAMPs determine the downstream signaling outcome of sept
192 ating into injured tissues tonically release DAMPs, including the high mobility group box 1 protein (
193 ent with the notion that osteolysis releases DAMPs from bone matrix, pharmacologic inhibition of bone
194 ity and, potentially, tolerance that renders DAMPs nonredundant players in responses to both sterile
197 of defense against atherosclerosis-specific DAMPs, and engage adaptive immune responses, provided by
199 h, but the relative contribution of specific DAMPs, including high-mobility group box 1 (HMGB1), is i
200 protein recognize common oxidation-specific DAMPs, such as oxidized phospholipids and oxidized chole
202 ll-like receptors (TLRs) that recognize such DAMPs and PAMPs, or the downstream effector molecules th
204 ablishes HMGB1 as a bona fide and targetable DAMP that selectively triggers a neutrophil-mediated inj
209 eficient in the IL-1 family receptor for the DAMP, IL-33 (called ST2), displayed reduced intestinal T
211 ur opinion that these function to remove the DAMP (ATP) released by host cells in response to schisto
215 se initiated by the accumulation of OSE type DAMPs and perpetuated by maladaptive response of the inn
217 ricted receptor specific for an unidentified DAMP that is exposed by necrotic cells and is necessary
221 LPS-primed glial cells were stimulated with DAMPs under acidic conditions (pH 6.2), the predominant
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