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 where the innate immune system sets-off the danger signal.

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

9 a range of microbial stimuli and endogenous danger signals.

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

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

12 n inflammasome complex induced by sensing of danger signals.

13 nts of inflammatory cytokines in response to danger signals.

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

15 t can potentially alert host defense against danger signals.

16 ated in response to microbial and endogenous danger signals.

17 response to pathogen-derived and endogenous danger signals.

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

19 iple hits involving endogenous and exogenous danger signals.

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

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

22 to particulate damage-associated endogenous danger signals.

23 zed that eosinophils may react to endogenous danger signals.

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

25 r receptors for infectious and noninfectious danger signals.

26 vigorous innate immune response upon sensing danger signals.

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

28 uence their basal functions and responses to danger signals.

29 might elaborate immune-activating endogenous danger signals.

30 y innate and Ag-specific immune responses to danger signals.

31 s, especially if associated with appropriate danger signals.

32 ce of correct presentation and costimulatory/danger signals.

33 nized Staphylococcus aureus and inflammatory danger signals.

34 eath in response to pathogens and endogenous danger signals.

35 vated in response to microbial infection and danger signals.

36 ialylated receptors that recognize exogenous danger signals.

37 receptor that senses microbes and endogenous danger signals.

38 olled and typically requires two consecutive danger signals.

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

40 to initiate inflammatory response to various danger signals.

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

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

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

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

45 y reflect a dysregulated response to immune "danger" signals.

46 countered in the absence of inflammation or "danger" signals.

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

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

49 ntigen presentation and providing endogenous danger signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

63 l activators of the innate immune system, or danger signals, also inhibit apoptosis and proliferation

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

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

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

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

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

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

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 Thus endogenous danger signals and exogenous PAMPs elicit similar respon

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

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

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

78 nhibition (analgesia) is produced by learned danger signals and inhibited by learned safety signals (

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

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

81 s, also inhibit apoptosis and proliferation, danger signals and necrotic cells differ from apoptotic

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

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

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

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

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

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

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

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

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

100 Danger signals are thought to act by stimulating dendrit

101 -1beta release, even in the presence of both danger signals, are needed to protect from collateral da

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

103 In the absence of a danger signal, artificially provided by adjuvants, most

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

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

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

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

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

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

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

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

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

113 However, when SAg was administered with a danger signal at the time of OX40 ligation, a synergisti

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 detected, like bacterial or viral DNA, as a danger signal by the vertebrate immune system.

119 indings suggest a novel function for B7-1 in danger signaling by nonimmune cells.

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

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

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

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

138 ge or abnormal death - and also by exogenous danger signals elaborated by pathogens.

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

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

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

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

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

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

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

151 ascular endothelial cells must also react to danger signals from the surrounding tissue and immediate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 Spinal morphine mimics learned danger signals in producing analgesia, which is inhibite

167 e opposing tendencies of apoptotic cells and danger signals in promoting tolerance vs immunity.

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

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

170 1, and plays a role in sensing pathogens and danger signals in the innate immune system.

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

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

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

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

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

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

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

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

179 One potential danger signal is ATP, high concentrations of which stimu

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

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

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

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

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

185 cells are capable of providing the necessary danger signals, likely through increased surface express

186 long-lived CD4 T cell memory in vivo: Ag, a danger signal (LPS), and OX40 engagement.

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

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

189 h an ancestral immunological role of gp96 as danger-signaling molecule.

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

191 malian cells have also been found to release danger signals of unknown identity.

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

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

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

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

196 Endogenous danger signals, or damage-associated molecular patterns

197 Danger signals, or pathogen-associated molecular pattern

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

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

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

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

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

203 roteases, and suggest that the triggering of danger signal receptors by exogenous pathogen-derived mo

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

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

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

207 how that uric acid is a principal endogenous danger signal released from injured cells.

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

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

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

211 Endogenous danger signals released from necrotic cells are thought

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

213 mune responses, can be induced by endogenous danger signals - released by tissues undergoing stress,

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

215 ls, which when engaged in conjunction with a danger signal, rescues Ag-stimulated effector cells from

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

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

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

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

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

221 covered family of intracellular pathogen and danger signal sensors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 gnize conserved microbial Ags and endogenous danger signals that may be triggered by injury, we wante

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

250 Some endogenous danger signals that recently have been discovered are he

251 us indicate that kinin peptides can serve as danger signals that trigger dendritic cells to produce I

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

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

254 rt the hypothesis that CpG DNA motifs are a "danger signal" that activates protective innate immune d

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

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

257 e elaboration and sensing of proinflammatory danger signals, thereby shifting the balance from activa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 mal tissue components therefore can serve as danger signals to enhance the immunogenicity of apoptoti

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

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

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

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

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

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

279 Microbes or danger signals trigger inflammasome sensors, which induc

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

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

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

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

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

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

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

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

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

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

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

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