ライフサイエンスコーパス: danger signal

1 ted not only by pathogens but by endogenous 'danger signals'.

2 but impaired when one stimulus was a learned danger signal.

3 y immune cells as an inflammasome-activating danger signal.

4 screte traces of a threat into a discernible danger signal.

5 terstitium, uromodulin becomes an endogenous danger signal.

6 cellular Hsp72 as an endogenous adjuvant and danger signal.

7 olled and typically requires two consecutive danger signals.

8 d NLRP3 to sense pathogen invasion and other danger signals.

9 to initiate inflammatory response to various danger signals.

10 lycan fragments in the host cell cytosol, as danger signals.

11 e variety of endogenous and pathogen-derived danger signals.

12 spase-1 in response to diverse intracellular danger signals.

13 a range of microbial stimuli and endogenous danger signals.

14 microbial pathogens as well as host-derived danger signals.

15 o the circulation and tissues in response to danger signals.

16 n inflammasome complex induced by sensing of danger signals.

17 phages provide defence against pathogens and danger signals.

18 ld explain how NLRP3 is activated by diverse danger signals.

19 t can potentially alert host defense against danger signals.

20 microbial capacity, which is up-regulated by danger signals.

21 response to pathogen-derived and endogenous danger signals.

22 immature, suppressive, and respond poorly to danger signals.

23 iple hits involving endogenous and exogenous danger signals.

24 beta, is induced by endogenous and exogenous danger signals.

25 urate (MSU) crystals as important endogenous danger signals.

26 to particulate damage-associated endogenous danger signals.

27 zed that eosinophils may react to endogenous danger signals.

28 r receptors for infectious and noninfectious danger signals.

29 vigorous innate immune response upon sensing danger signals.

30 pathways, and occurs even in the absence of danger signals.

31 might elaborate immune-activating endogenous danger signals.

32 (NODs) can also recognize a broader array of danger signals.

33 receptor that senses microbes and endogenous danger signals.

34 nts of inflammatory cytokines in response to danger signals.

35 ated in response to microbial and endogenous danger signals.

36 uence their basal functions and responses to danger signals.

37 nized Staphylococcus aureus and inflammatory danger signals.

38 ates the capacity of monocytes to respond to danger signals.

39 eath in response to pathogens and endogenous danger signals.

40 vated in response to microbial infection and danger signals.

41 ialylated receptors that recognize exogenous danger signals.

42 me senses lysosomal damage as an endogenous 'danger' signal.

43 ve immunity in response to pathogen-derived "danger" signals.

44 ain involves ethanol activation of HMGB1/TLR danger signaling.

45 l-like receptor (TLR) family associated with danger signaling.

46 ssion of immune responses in the absence of "danger signals."

47 sensor of the system and a major source of "danger signals"; (2) the endothelium as an internal sens

48 ulus was neutral and the other was a learned danger signal, acquisition and extinction of the associa

49 nflammatory cytokines for the propagation of danger signals across the tissue at large.

50 Together, these danger signals activate antigen-presenting cells (APCs)

51 Pathogens and cellular danger signals activate sensors such as RIG-I and NLRP3

52 n of immature IL-1beta, and then endogenous "danger" signals activate innate immune signaling complex

53 Necrotic cells release danger signals, activating innate immune pathways and tr

54 locking signaling by the putative endogenous danger signal adenosine, which can be released during in

55 lowing transplantation, the proinflammatory "danger signal" adenosine triphosphate (ATP) is released

56 ress TLRs and other PRRs that directly sense danger signals after injury or during infection, leading

57 myelin on BCVs may therefore act as an early danger signal alerting the cell to imminent bacterial in

58 In doing so, LMW HA acts as an endogenous danger signal alerting the immune system of a breach in

59 x (MHC) class I-like molecules that act as a danger signal alerting the immune system to the presence

60 ic environment represents a novel endogenous danger signal alerting the innate immunity.

61 Acidic pH represents a novel danger signal alerting the innate immunity.

62 iosis surgery, this study shows that soluble danger signals, among them interleukin-1beta, increase b

63 TLRs), inflammatory cytokines, and putative "danger" signals, among other signaling pathways, in trig

64 It may act as a danger signal, an antioxidant, or a substrate for heme p

65 dsRNA in biochemical assays to eliminate the danger signal and inhibit the innate immune response.

66 rystalline cholesterol acts as an endogenous danger signal and its deposition in arteries or elsewher

67 Kidney injury implies danger signaling and a response by the immune system.

68 serum amyloid A (SAA) is a host response to danger signals and a clinical indication of inflammation

69 lf-derived autoantigens and pathogen-derived danger signals and antigens.

70 n the future is to modulate the intensity of danger signals and consequently the systemic inflammator

71 Nlrp3 inflammasome senses obesity-associated danger signals and contributes to obesity-induced inflam

72 rations, but importantly also in response to danger signals and cytokines.

73 esulting in decreased intragraft exposure to danger signals and dampened alloimmune responses.

74 broad range of microbial motifs, endogenous danger signals and environmental irritants, resulting in

75 Thus endogenous danger signals and exogenous PAMPs elicit similar respon

76 Some of the NLRs also sense nonmicrobial danger signals and form large cytoplasmic complexes call

77 he Western lifestyle and diet promote innate danger signals and immune responses through production o

78 s cells (LCs) are epithelial APCs that sense danger signals and in turn trigger specific immune respo

79 RNA sensors recognize virus-derived dsRNA as danger signals and initiate innate immune responses.

80 epithelia express receptors that respond to danger signals and initiate repair programs.

81 complexes that sense intracellular microbial danger signals and metabolic perturbations.

82 these receptors recognize microbes and other danger signals and of how they activate inflammatory sig

83 These results provide a mechanism by which danger signals and particulate matter mediate inflammati

84 r the activation of caspase-1 in response to danger signals and particulate matter.

85 to innate immunity by sensing environmental danger signals and producing proinflammatory cytokines.

86 ne cells and hepatocytes recognize microbial danger signals and regulate immune responses.

87 n the ability of MCs to detect pathogens and danger signals and release a unique panel of mediators t

88 tively inhibit cellular recognition of viral danger signals and the subsequent cellular response to t

89 Inflammasomes sense exogenous and endogenous danger signals and trigger IL-1beta and IL-18 activation

90 l damage/disease and so P2X7Rs respond to a "danger" signal and are not normally active.

91 Inflammasomes respond to pathogen or tissue "danger" signals and assemble into multiprotein "machiner

92 much attention as the sensor of endogenous "danger signals" and mediator of "sterile inflammation" i

93 oimmunity induction by persistent endogenous danger signal, and (ii) autoantigenic stimulation with s

94 ll fusion through micronuclei formation as a danger signal, and consequently limits aberrant cell div

95 contact with peripheral antigens, cytokines, danger signals, and immune cells travelling from periphe

96 at highlight how cellular stress, endogenous danger signals, and innate immune activation promote the

97 sentinel functions, sampling for antigen and danger signals, and mature DCs (mDCs), which exhibit enh

98 re made, their function in infections and as danger signals, and their emerging importance in autoimm

99 (TLRs) are critical receptors to respond to danger signals, and their functions are relevant in the

100 tforms assembled in response to infection or danger signals, and they regulate the activation of casp

101 essive release of inflammatory cytokines and danger signals are linked to an increasing spectrum of i

102 livery systems for antigens and/or molecular danger signals are promising adjuvants capable of promot

103 -1beta release, even in the presence of both danger signals, are needed to protect from collateral da

104 es tumor epitopes and provides costimulatory danger signals, arming the virus with immunostimulatory

105 Pathogen- and injury-related danger signals as well as cytokines released by immune c

106 nd release of pro-inflammatory cytokines and danger signals as well as pyroptosis in response to infe

107 inflammasome can be activated by endogenous "danger signals" as well as compounds associated with pat

108 Thus, in the absence of danger signals, as is often the case in a tumor-bearing

109 iles were regulated by external and internal danger signals, as well as whether bacteria were membran

110 Here, we demonstrated that danger signals associated with dying cells are not suffi

111 release in response to TLR4 detection of the danger signals associated with infections of the central

112 In this study, we show that early "danger" signals associated with transplantation lead to

113 Emerging evidence has also shown that early "danger signals"' associated with ischemia-reperfusion in

114 The proinflammatory danger signal ATP, released from damaged cells, is degra

115 inergic receptor (P2X7) by the inflammatory "danger" signal ATP induces PAD2 activity and robust prot

116 nduces acute extracellular accumulation of a danger signal, ATP; autocrine ATP sustains increases in

117 nocyte proinflammatory responses to systemic danger signals, but attenuating macrophage cytokine resp

118 ic protein complexes that respond to diverse danger signals by activating caspase-1.

119 e immune responses to invading pathogens and danger signals by activating caspase-1.

120 unctions, the local release of cytokines and danger signals by dying radiosensitive cells, and altere

121 immune cells and the release of antigens and danger signals by malignant cells killed by chemotherapy

122 epend on timely recognition of pathogenic or danger signals by multiple cell surface or cytoplasmic r

123 NLRP3 inflammasome responds to microbes and danger signals by processing and activating proinflammat

124 inal cord injury (SCI) causes the release of danger signals by stressed and dying cells, a process th

125 Recognition of these components as danger signals by the host activates immune responses le

126 Such viral vectors, recognized as danger signals by the host immune system, activate dendr

127 al memory of antigen, whereas recognition of danger signals by the innate immune system determines th

128 ilitates the sensing of pathogen-associated "danger" signals by intracellular receptors.

129 be leveraged by immunomodulators such as the danger signal calreticulin.

130 in response to both exogenous and endogenous danger signals can lead to the assembly of cytoplasmic i

131 nflammasomes, which respond to pathogens and danger signals, cleave IL-1beta cytokines via caspase-1.

132 orchestrating immune responses and sending 'danger' signals, complement contributes substantially to

133 These findings support the concept that danger signals contribute to the T cell responses to cel

134 DNA in the cytoplasm of mammalian cells is a danger signal detected by the DNA sensor cyclic-GMP-AMP

135 tein in myeloid cells, acts as an endogenous danger signal, driving inflammation and aggravating tiss

136 o pathogens, microbial toxins, or endogenous danger signals, EC responses are polymorphous, heterogen

137 ead cells, and other substances perceived as danger signals; efflux cholesterol to high-density lipop

138 d by innate pattern recognition receptors as danger signals either directly or through production of

139 For this study, we used representative danger signals (elicitors) belonging to the classes of t

140 tors (PRRs) function as sensors of microbial danger signals enabling the vertebrate host to initiate

141 ulence factors of L. pneumophila, the potent danger signal flagellin and the translocated Dot/Icm typ

142 Citrulline is a potent indicator as a danger signal for ACR, being an exclusionary, noninvasiv

143 olesterol crystals acted both as priming and danger signals for IL-1beta production.

144 owever, murine macrophages require a second "danger signal" for the inflammasome-driven maturation of

145 which occurs during inflammation) acts as a 'danger signal' for the meningococcus, enhancing its defe

146 T cell homeostasis and responses to external danger signals from "sterile" inflammation remain poorly

147 inhibiting the release of self antigens and danger signals from apoptotic cell-derived constituents

148 dendritic cell subset specialized in sensing danger signals from bacteria and tissue breakdown.

149 the cell surface facilitate the detection of danger signals from diverse pathogens and initiate a ser

150 enic phenotype, despite constant exposure to danger signals from food and microbes.

151 Furthermore, PA triggers the release of danger signals from hepatocytes in a caspase-dependent m

152 ceptors are present in nociceptors to detect danger signals from infections.

153 Release of molecular danger signals from injured cell mitochondria (mitochond

154 nse against infection after host cells sense danger signals from microbes.

155 of actin polymerization can remove potential danger signals from the system and prevents monocyte IL-

156 itic cells (DCs) by inducing the release of "danger" signals from dying tumor cells.

157 rols inflammatory responses to intracellular danger signals generated by pathogens, is both activated

158 Release of endogenous danger signals has been linked to adjuvanticity; however

159 adipocytes may function as an immunological "danger signal." Here we show that endogenous oils of hum

160 ROS oxidized the potential danger signal high-mobility group box-1 protein (HMGB1)

161 were cellular damage, thereby releasing the danger signal HMGB-1 in the brain to prime microglia by

162 ced lung inflammation through release of the danger signal HMGB1.

163 rganisms (i.e., intra-amniotic infection) or danger signals (i.e., sterile IAI) has been implicated i

164 The proinflammatory danger signal IL-33, which is released from damaged or d

165 Mammalian immune responses are initiated by "danger" signals--immutable molecular structures known as

166 n and suggest a key role for this endogenous danger signal in driving adaptive immunity in erosive jo

167 ugh cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1beta

168 in chemotherapeutic drugs elicit immunogenic danger signals in dying cancer cells that can incite pro

169 ey role in orchestrating tissue responses to danger signals in NASH.

170 Adenine nucleotides induce danger signals in T cells via purinergic receptors, rais

171 Intracellular pathogens and endogenous danger signals in the cytosol engage NOD-like receptors

172 1, and plays a role in sensing pathogens and danger signals in the innate immune system.

173 tilize TLRs and other PRR pathways to detect danger signals in their environment.

174 activity, which functions to generate local "danger signals" in nearby airway epithelium.

175 These agonists offer a means of providing "danger signals" in order to activate the immune system t

176 These hepatocyte-derived danger signals, in turn, activate inflammasome, IL-1beta

177 Detection of various danger signals, including microbe-associated molecular p

178 In premature infants, danger signal-induced DC activation may promote proinfla

179 Following recognition of pathogens and danger signals, inflammasomes assemble and recruit and a

180 spinal cord injury (SCI) rapidly produce the danger signal interleukin (IL)-1alpha, which triggers ne

181 nt T cell antigen receptor translates innate danger signals into iNKT cell activation.

182 operty of HSPCs that enables them to convert danger signals into versatile cytokine signals for the r

183 , flagellin)-derived, NF-kappaB-stimulating "danger" signal into the large stress protein or chaperon

184 t that the release of HMGB1 as an endogenous danger signal is important for priming an adaptive immun

185 al that extracellular ATP acting as an early danger signal is responsible for the activation of Duox1

186 ed and host gene expression induced by these danger signals is vital to understanding virus-host inte

187 red organ to systemic circulation, so-called danger signals, is growing to include multiple metabolit

188 recognizing certain nonmicrobial originated 'danger signals' leading to caspase-1 activation and subs

189 Therefore, danger signals may drive sterile inflammation, such as t

190 ts memory CD8(+) T cells as early sensors of danger signals, mediating protective immunity both throu

191 The epithelial cell-derived danger signal mediators thymic stromal lymphopoietin (TS

192 mobility group protein 1 (HMGB1), a sterile danger signal molecule, and osteopontin (OPN), a multifu

193 nt study, we investigated how the endogenous danger signal monosodium urate (MSU) crystals can alter

194 llular damage, may function as an endogenous danger signal or alarmin, similar to IL-1alpha or high-m

195 t does not require the presence of microbial danger signals or alarmins associated with cytopathic da

196 can activate the immune system by providing danger signals or they may downregulate immune and infla

197 r sites, where it functions as an endogenous danger signal, or alarmin, in response to tissue damage.

198 Endogenous danger signals, or damage-associated molecular patterns

199 Danger signals, or pathogen-associated molecular pattern

200 inels for the immune system, MG also detect "danger" signals (pathogenic or traumatic insult), become

201 L-33) is implicated as an epithelium-derived danger signal promoting Th2-dependent responses in asthm

202 igands include bacterial cell wall proteins, danger signaling proteins, and intracellular proteins su

203 Uric acid (UA) is an endogenous danger signal recently identified to be released from dy

204 ossess danger sensing pathways composed of a danger signal receptor and corresponding signal transduc

205 ested to promote immunogenicity by acting as danger signals recognized by dendritic cells (DC) facili

206 tracellular sensing of pathogens, as well as danger signals related to cell injury.

207 Necroptosis and subsequent danger signal release is a novel mechanism of injury fol

208 ssue types and detect extracellular ATP as a danger signal released from dying cells.

209 These studies show that IL-1alpha is a key danger signal released from necrotic cells to trigger CX

210 Interleukin-1alpha (IL-1alpha) is a key danger signal released upon necrosis that exerts effects

211 lts reveal that in addition to their role as danger signals released from dead cells, IL-1 family cyt

212 Understanding the nature of endogenous danger signals released from dying cells may aid in a be

213 Endogenous danger signals released from necrotic cells are thought

214 s on the cell surface to detect host-derived danger signals released in response to attacks by pathog

215 nctions, have evolved extracellular roles as danger signals released in response to cell lysis, apopt

216 At the same time, danger signals released into the circulation by damaged

217 y was ascribed primarily to dsDNA and other "danger" signals released from laser-damaged skin cells.

218 ansport in macrophages constitutes a general danger signal required for NLRP3-related inflammation.

219 ts as an alarmin, initiating and propagating danger signals resulting from tissue injury or inflammat

220 The nature of the inflammasome-activating danger signal(s) in adipose tissue in obesity remains to

221 The NLRP3 inflammasome acts as a danger signal sensor that triggers and coordinates the i

222 nt domain)), caspase-1 activation by another danger-signaling sensor NLRP1 does not require ASC becau

223 ct with various PYD-containing intracellular danger signal sensors and PYD-only proteins.

224 covered family of intracellular pathogen and danger signal sensors.

225 onents by acting as a molecular glue between danger-signal sensors and procaspase-1.

226 These findings suggest that Prx1 may act as danger signal similar to other TLR4-binding chaperone mo

227 e initiation phase of acute GvHD, endogenous danger signals such as ATP are released and inform the i

228 ress or injury induces release of endogenous danger signals such as ATP, which plays a central role i

229 amma and suggest a revised paradigm in which danger signals such as IL-33 are crucial amplifiers of i

230 ent and discriminate between homeostatic and danger signals such as modified components of the extrac

231 macrophages are activated by lipid derived "danger signals" such as ceramides and palmitate and prom

232 signals are up-regulated in the presence of "danger signals" such as LPS or viral nucleic acids.

233 NLRP3 inflammasome activation in response to danger signals, such as a hypotonic environment, largely

234 Taken together, inflammatory cues and danger signals, such as bone and implant particles exace

235 al lymphopoietin, and GM-CSF, and endogenous danger signals, such as high-mobility group box 1, uric

236 of proinflammatory signaling and release of danger signals, such as HMGB1.

237 active oxygen species stress associated with danger signals, such as induction of cell-surface calret

238 on is unclear and the involvement of another danger signal system has been proposed.

239 ty, a system built for ubiquitous sensing of danger signals, tend to generate systemic autoimmunity.

240 ating of the intestine may be perceived as a danger signal that activates an immune fight-and-flight

241 DNA in the cytoplasm of mammalian cells is a danger signal that activates innate immune responses; ho

242 rom the nucleus or mitochondria represents a danger signal that alerts the host immune system(1).

243 with crystalline cholesterol, an endogenous danger signal that contributes to atherogenesis.

244 Interleukin (IL)-33 is a danger signal that is a critical regulator of chronic in

245 Extracellular ATP is an endogenous danger signal that is known to activate inflammatory res

246 hat TLR9 can respond to mitochondrial DNA, a danger signal that is released upon tissue injury, we ex

247 results identify tenascin-C as an endogenous danger signal that is upregulated in SSc and drives TLR4

248 ransplantation, IL-6 functions as a systemic danger signal that overcomes constitutive immune suppres

249 ndogenous, concentration-dependent pulmonary danger signal that primes and activates the NLPR3 inflam

250 DNA in the cytoplasm of mammalian cells is a danger signal that triggers host immune responses such a

251 eflex action that is sufficient to provide a danger signal that triggers regional immunity to fight a

252 lytic cleavage represents an ancient type of danger signaling that may be highly relevant for the pri

253 Dead cells also release danger signals that activate dendritic cells and promote

254 Injured cells release danger signals that alert the host to cell death.

255 med toward excess nutrients and the numerous danger signals that appear in a variety of chronic infla

256 s immunogenic and the tumors lack the potent danger signals that are characteristic of viruses.

257 Viral infection activates danger signals that are transmitted via the retinoic aci

258 s procoagulant activity, which may result in danger signals that drive the immune response.

259 communication pathways involving endogenous danger signals that have recently been argued to facilit

260 Cells undergoing necrosis release endogenous danger signals that possess proinflammatory potential.

261 hepatocytes exposed to saturated FAs release danger signals that trigger inflammasome activation in i

262 The dying cells in the MTZs send 'danger' signals that attract a large number of antigen-p

263 T-cell responses may be shaped by sterile "danger signals" that are constituted by damage-associate

264 s to abnormal tissue turnover or damage as a danger signal; the signaling indicator ligands would ref

265 in vivo in response to infections and other danger signals, these findings may have important implic

266 Upon recognition of such "danger" signals, they undergo dynamic reprogramming of g

267 d mount a variety of integrated responses to danger signals through intricate chemical messengers.

268 neutrophils and macrophages via signaling of danger signals through NETs.

269 These cells recognize danger signals through receptors capable of inducing spe

270 T cells can also directly recognize danger signals through the expression of TLRs.

271 ures from intact cells, which could act as a danger signal to activate the immune system.

272 Necrotic cells release HMGB1 as a danger signal to activate the immune system.

273 racellular ATP has been proposed to act as a danger signal to alert the immune system of cell damage.

274 ighlight the role of this self-molecule as a danger signal to alert the NK cell network.

275 g single TLR ligands with a non TLR-mediated danger signal to cooperatively induce distinct DC proper

276 ular adenosine triphosphate (ATP) binds as a danger signal to purinergic receptor P2X7 and promotes i

277 They provide a danger signal to the mammalian immune system that trigge

278 mediate innate immune signaling or generate danger signals to activate immune cells.

279 and subsequently present cancer antigens and danger signals to activate the resident dendritic cells

280 ction by sensing pathogens and communicating danger signals to noninfected neighbors; however, little

281 vHD, which could be exploited when targeting danger signals to prevent GvHD.

282 death that causes the subsequent release of danger signals to propagate and perpetuate inflammatory

283 at patients generalize conditioned fear from danger signals to safety signals especially when the two

284 lammasomes and link microbial and endogenous danger signals to the activation of caspase-1.

285 ammasome that link microbial and endogenous 'danger' signals to caspase-1 activation.

286 Microbes or danger signals trigger inflammasome sensors, which induc

287 Intracellular pathogens and danger signals trigger the formation of inflammasomes, w

288 s related to innate immunity and response to danger signals triggered by activating transcription fac

289 ndings identify IL-1alpha as a crucial early danger signal triggering post-MI inflammation.

290 tal immune sensor that recognizes endogenous danger signals triggering sterile inflammation.

291 NLRP3 inflammasome assembles in response to danger signals, triggering self-cleavage of procaspase-1

292 sponse to microbial components or endogenous danger signals, triggers caspase-1-mediated maturation a

293 ablished local inflammatory response to AKI, danger signaling unleashes a cascade of precisely timed,

294 Thus, depending on the original danger signal, vascular DCs edit the emerging immune res

295 s of sterile inflammation, which established danger signaling via pattern recognition receptors as a

296 Thus, in addition to its role as a danger signal, which occurs when the cytokine is passive

297 eATP is generally considered as a classical danger signal, which stimulates immune responses in the

298 omeostasis by a TLR7-dependent nucleic acid "danger" signal, which may signify viral infection or loc

299 iptional response to a microbial stimulus or danger signal with a high degree of cell type and stimul

300 Integrating metabolic, oxygen, or danger signals with inputs from other organelles, as wel