ライフサイエンスコーパス: inflammasome

1 hypothesized that Tat could prime the NLRP3 inflammasome.

2 and the assembly and activation of the NLRP3 inflammasome.

3 ese findings suggest sUA activates the NLRP3 inflammasome.

4 e ASC speck is critical for signaling by the inflammasome.

5 e of Tat in priming and activating the NLRP3 inflammasome.

6 action of a molecular assembly known as the inflammasome.

7 corroborating a pathogenic role of the Nlrp3 inflammasome.

8 ory responses, with an emphasis on the NLRP3 inflammasome.

9 y is Aim2, which encodes an activator of the inflammasome.

10 l player in the negative regulation of NLRP3 inflammasome.

11 known to blunt activation of the human NLRP3 inflammasome.

12 ing cascade as well as inactivation of NLRP3 inflammasome.

13 n crystalized, is able to activate the NLRP3 inflammasome.

14 autoinflammation via activation of the NLRP3 inflammasome.

15 he activation and stabilization of the NLRP3 inflammasome.

16 pha in response to particulate activators of inflammasome.

17 components of a multiprotein complex called inflammasome.

18 ation of the multiprotein complex NLRP3-type inflammasome.

19 receptors such as NOD-like receptors, NLRP3 inflammasomes.

20 -kappaB-dependent transcription and multiple inflammasomes.

21 gest that ZIKV transcription is regulated by inflammasomes.

22 IPK3 can also mediate apoptosis and regulate inflammasomes.

23 ctivated by various protein platforms called inflammasomes.

24 The NLRP3 inflammasome, a caspase-1 activation platform, plays a k

25 cids to influence inflammation and the NLRP3 inflammasome across numerous metabolic tissues in the bo

26 LRC4 and NLRP3, which normally form distinct inflammasomes, activate an LPC-induced inflammasome and

27 Consistent with this, deletion of GDF3 in inflammasome-activated macrophages improved lipolysis by

28 y assessment of IL-1beta mRNA expression and inflammasome activation (ASC oligomers and mature IL-1be

29 s support a role for mitochondrial damage in inflammasome activation and CKD and suggest mitochondria

30 aicalein reduced NOD-like receptor 3 (NLRP3) inflammasome activation and downstream interleukin-1beta

31 vels, we observed a correlation between sUA, inflammasome activation and fibrosis.

32 trate that P2X5 is required for ATP-mediated inflammasome activation and IL-1beta production by OCs,

33 age by Yersinia translocon proteins promotes inflammasome activation and implicate GBPs as key regula

34 laque inflammation by inhibition of lesional inflammasome activation and reduced experimental atheros

35 own or pharmacological inhibitor compromised inflammasome activation and subsequent production of bio

36 In the past several years, inflammasome activation and subsequent signal transducti

37 NLRP1 promotes melanoma growth by enhancing inflammasome activation and suppressing apoptotic pathwa

38 cts from IRI by restricting mTORC1-dependent inflammasome activation and that mimicking biased aPC PA

39 am with diverse immune functions and promote inflammasome activation and the production of IL-1beta a

40 DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL

41 er, the molecular mechanisms responsible for inflammasome activation are unknown.

42 ential for TcpB to subvert the non-canonical inflammasome activation as a TcpB(G158A) mutant failed t

43 n of microtubule dynamics orchestrates NLRP3 inflammasome activation by controlling its transport to

44 Inhibition of inflammasome activation by the S.

45 These results demonstrate that Nrf2-related inflammasome activation can promote CKD symptoms via inf

46 athy (DR), mitophagy dysregulation and NLRP3 inflammasome activation exist, which cause premature cel

47 bitors uncouple lipid-induced ER stress from inflammasome activation in both mouse and human macropha

48 We investigated the role of inflammasome activation in cholangiocyte response to inj

49 However, the mechanism underlying inflammasome activation in CKD remains elusive.

50 ow that AIM2 is dispensable for DNA-mediated inflammasome activation in human myeloid cells.

51 In vitro aPC inhibited inflammasome activation in macrophages, cardiomyocytes,

52 of L. amazonensis infection is critical for inflammasome activation in macrophages.

53 n and demyelination, elicits NLRP3 and NLRC4 inflammasome activation in microglia and astrocytes, whi

54 n and fibrosis induced by constitutive NLRP3 inflammasome activation in myeloid-derived cells.

55 Accordingly, inflammasome activation in response to L. amazonensis is

56 ffects of ANDRO in NASH and its influence on inflammasome activation in this setting.

57 These findings support the concept that inflammasome activation is connected to seeding and spre

58 Inflammasome activation is critical for the host's defen

59 tion followed by ATP or nigericin treatment, inflammasome activation is enhanced in monocytes from WA

60 While inflammasome activation is essential for host defense, d

61 Inflammasome activation leads to the activation of caspa

62 Pharmacological inhibition of NLRP3 inflammasome activation may offer a new option in the tr

63 ting that restoring mitophagy and inhibiting inflammasome activation may serve as novel targets for t

64 e insight into the mechanisms by which NLRC4 inflammasome activation mediates auto-inflammatory disea

65 hilic inflammation and neutrophil-associated inflammasome activation might represent interacting path

66 NLR family pyrin domain containing 3 (NLRP3) inflammasome activation often acts as a rate-limiting st

67 Kinetic in vivo analyses revealed that Nlrp3 inflammasome activation preceded myocardial injury and a

68 nterstitial sodium, cytokine production, and inflammasome activation promote immune activation in hyp

69 Inflammasome activation requires two signals, both of wh

70 these data demonstrate that oxLDL ICs induce inflammasome activation through a separate and more robu

71 with pronounced host antiviral response and inflammasome activation together with accelerated lung r

72 aP2 regulates macrophage redox signaling and inflammasome activation via control of UCP2 expression.

73 Insulin sensitivity and Nlrp3 inflammasome activation were monitored in wild-type (WT)

74 se pyroptosis (ie, cell death resulting from inflammasome activation) is typically observed in IRI, w

75 defective mitophagy, associated exaggerated inflammasome activation, cell death, and IL-18 secretion

76 s a conduit for mitochondrial-damage-induced inflammasome activation, expand the immune-sensing reper

77 interleukin 1beta (IL-1beta), in response to inflammasome activation, is ablated in FABP4/aP2(-/-) ma

78 ce support the critical role of Dectin-1 for inflammasome activation, restriction of parasite replica

79 l accumulation (ie, foam cell formation) and inflammasome activation, the extracellular lipoprotein p

80 namic B-repeat domain of M1 was critical for inflammasome activation, which involved K(+) efflux and

81 emporally, cGAMP induction of IFN-I precedes inflammasome activation, which then occurs when IFN-I is

82 tion may normalize mitophagic flux and NLRP3 inflammasome activation, which will prevent or slow down

83 elates with NLRP3 abundance and the state of inflammasome activation.

84 and caspase-1 processing, key events during inflammasome activation.

85 tory responses via the complement system and inflammasome activation.

86 iolipin release may trigger abacavir-induced inflammasome activation.

87 zler syndrome is associated with upregulated inflammasome activation.

88 patterns to the host cytosol with consequent inflammasome activation.

89 sists long after ischemia to sustain chronic inflammasome activation.

90 impairs NLRP3 spatial arrangement and limits inflammasome activation.

91 lated that aPC ameliorates IRI by inhibiting inflammasome activation.

92 a cleavage upon NLRP3, but not AIM2 or NLRC4 inflammasome activation.

93 lly cytokines related to NF-kappaB and NLRP3 inflammasome activation.

94 f endogenous Alu-retroelement RNA, and NLRP3-inflammasome activation.

95 ow that BTK is a critical regulator of NLRP3 inflammasome activation: pharmacologic (using the US Foo

96 hibitors, identifying abacavir as a specific inflammasome activator.

97 tor of inflammatory cytokines, as well as an inflammasome activator.

98 living macrophages that have been exposed to inflammasome activators, such as bacteria and their prod

99 L-1alpha and IL-1beta in vivo in response to inflammasome activators.

100 Dysregulation of autophagy and inflammasome activity contributes to the development of

101 r, to date, few proteins that regulate NLRP3 inflammasome activity in human primary immune cells have

102 Here we analyzed the impact of aPC on inflammasome activity in myocardial and renal IRIs.

103 AIM2 deficiency rescues the increased inflammasome activity observed in Ch25h(-/-).

104 The effect of TRX80 on NLRP3 inflammasome activity was evaluated by measuring the lev

105 that IL-18, the other cytokine triggered by inflammasome activity, is important in its own right.

106 anced local inflammation was due to enhanced inflammasome activity.

107 macrophages without evidence of spontaneous inflammasome activity.

108 Assembly of the inflammasome allows for the cleavage and activation of i

109 nsposable elements, which activate the NLRP3 inflammasome and additional downstream pathways that com

110 tinct inflammasomes, activate an LPC-induced inflammasome and are important in astrogliosis and micro

111 Therefore, the NLRP3 inflammasome and associated metabolic inflammation have

112 tochondrial DNA, resulting in Aim2 and NLRC4 inflammasome and caspase-I hyperactivation in cardiomyoc

113 Consistent with inflammasome and caspase-I hyperactivation, cardiomyocyt

114 te immune system in both diseases, including inflammasome and complement pathways.

115 or family, pyrin domain-containing 3 (NLRP3) inflammasome and concomitant IL-1beta responses occur in

116 eted from HCV-exposed macrophages, activates inflammasome and fibrosis markers in HSCs and that neutr

117 Expression of inflammasome and fibrosis-related genes in these cells w

118 In mice, cGAS/cGAMP amplify both inflammasome and IFN-I to control murine cytomegalovirus

119 ng IL-1beta The potential roles of the NLRP3 inflammasome and IL-1beta in the peritoneal membrane dur

120 nal TILs through the activation of the NLRP3 inflammasome and IL-23/IL-17 axis.

121 soluble form, could also activate the NLRP3 inflammasome and induce the production of IL-1beta.

122 gnancies and is a known agonist of the Nlrp3 inflammasome and inducer of inflammation.

123 PB1-F2 derived from H7N9 activates the NLRP3 inflammasome and induces lung inflammation and cellular

124 ammatory effect on CC via suppression of the inflammasome and liver X receptor activation.

125 ults in dysregulated activation of the NLRP3 inflammasome and production of IL-1beta.

126 x components function as DAMPs for the NLRP3 inflammasome and regulate osteoclast differentiation.

127 ation also induces the assembly of the NLRP3 inflammasome and the maturation and release of IL-1beta,

128 lls that have both inappropriately activated inflammasomes and enhanced replicative potential.

129 3 result in abnormal activation of the NLRP3 inflammasome, and cause the autosomal dominant systemic

130 nd actin regulation in the activation of the inflammasome, and in human autoinflammation.

131 regulates expression, activity of the NLRP3 inflammasome, and its signaling pathway.

132 MLKL is an endogenous activator of the NLRP3 inflammasome, and that MLKL activation provides a mechan

133 asmic reticulum stress, the formation of the inflammasome, and the dysregulation of autophagy.

134 ammasome, more evidence has emerged that the inflammasome appears to play a pivotal role in the devel

135 nes 1205Lu and HS294T, indicating that NLRP1 inflammasomes are active in metastatic melanoma.

136 Inflammasomes are broadly expressed in haematopoietic an

137 Inflammasomes are cytosolic multi-molecular complexes th

138 Inflammasomes are cytosolic multiprotein complexes in ma

139 Inflammasomes are cytosolic multiprotein complexes that

140 Inflammasomes are cytosolic multiprotein complexes that

141 Inflammasomes are high-molecular-weight cytosolic comple

142 Inflammasomes are involved in gut homeostasis and inflam

143 Inflammasomes are key inflammatory signaling platforms t

144 Inflammasomes are multi-protein complexes that assemble

145 Inflammasomes are multiprotein complexes that sense path

146 Inflammasomes are multiprotein signaling complexes that

147 Here, we discuss recent insights into how inflammasomes are regulated to activate caspase-1 and im

148 rt, through SIRT3-directed blunting of NLRP3 inflammasome assembly and activation.

149 show that the PYD-only protein POP2 inhibits inflammasome assembly by binding to ASC and interfering

150 A critical outcome of inflammasome assembly is the activation of the cysteine

151 Inflammasome assembly requires the PYRIN domain (PYD)-co

152 P3 activation, showing that PP2A can license inflammasome assembly via dephosphorylating NLRP3 PYD.

153 wn about the interplay between autophagy and inflammasome assembly, although it is becoming evident t

154 tes the priming of Nlrp3, promotes Nlrp3-ASC inflammasome assembly, and results in the activation of

155 indicated a role of anion channels in NLRP3 inflammasome assembly, but their direct involvement has

156 te pyrin; this could potentially precipitate inflammasome assembly.

157 , consistent with K(+) loss being needed for inflammasome assembly.

158 d tissue inflammation and hyperproduction of inflammasome-associated cytokines.

159 An inflammasome-based surveillance machinery for Gram-negat

160 Our results demonstrate that treatment with inflammasome-blocking agents can significantly reduce th

161 Since QUC inhibited both NLRP3 and AIM2 inflammasomes but not NLRC4, we assessed ASC speck forma

162 lusion, QUC inhibits both the NLRP3 and AIM2 inflammasome by preventing ASC oligomerization and may b

163 protein stabilization and activation of the inflammasome by Toll-like receptor (TLR) agonism with ba

164 a multimeric signaling platform, termed the inflammasome, by members of the nucleotide-binding oligo

165 The NLRP3 inflammasome can indeed be activated in resident macroph

166 Inflammasomes can drive chronic inflammation in the cont

167 e roles and potential for targeting of NLRP3 inflammasome, caspase-1, and IL-1beta responses in exper

168 d molecular patterns that activate the NLRP3 inflammasome complex after tissue injury.

169 Autophagy and inflammasome complex assembly are physiological processe

170 hypothesized that NLRC3 might inhibit NALP3 inflammasome complex assembly.

171 with the assembly and activity of the NALP3 inflammasome complex by competing with ASC for pro-caspa

172 The inflammasome complex proteins ASC (apoptosis-associated

173 ilieu, orchestrated by the HIF-induced NLRP3 inflammasome complex, is a key determinant of acute thro

174 r protein that the initiates assembly of the inflammasome complex, is increased in colon biopsies fro

175 In vivo studies using wild-type and various inflammasome component knockout mice also revealed the p

176 entify a rheostat of DNA and RNA sensing-the inflammasome component NLRP14.

177 decreases in splenic mRNA expression of both inflammasome components (Nlrp3, Pycard, pro-Casp1) and p

178 nscriptional control or priming of canonical inflammasome components but, rather, occurred via SIRT3-

179 important transcriptional regulator of NLRP3 inflammasome components in murine inflammasomopathies.

180 Thus, targeting inflammasome components may ameliorate chronic inflammat

181 neumoniae-infected macrophages deficient for inflammasome components NLRP3, ASC (apoptosis speck-like

182 The inflammasome contains intracellular receptors that recog

183 Furthermore, such activation of NLRP3 inflammasome contributes to the induction of antigen-spe

184 t that XLA might result in part from genetic inflammasome deficiency and that NLRP3 inflammasome-link

185 ivered these lipids into the cell to promote inflammasome-dependent DC hyperactivation.

186 ion of the innate immune system and involves inflammasome-dependent formation of ASC specks in microg

187 kine secretion by monocytes, in a STING- and inflammasome-dependent manner.

188 mesothelial to fibroblastic transition in an inflammasome-dependent manner.

189 show that these novel GSDMD fusions execute inflammasome-dependent pyroptotic cell death in response

190 ection to characterize the role of the NLRP3 inflammasome during acute infection.

191 e receptor family, pyrin domain containing 3 inflammasome during acute pneumonia was confirmed in viv

192 sociated with eosinophilic SA, whereas NLRP3 inflammasome expression is highest in patients with neut

193 By generation of mice in which inflammasome expression is restricted to IECs, we descri

194 ungs had an increased number of macrophages, inflammasome expression remained restricted to macrophag

195 Mechanistically, enhanced NLRP3 inflammasome expression with elevated IL-1beta was a pre

196 nsically, indicating that MLKL-induced NLRP3 inflammasome formation and IL-1beta cleavage occur befor

197 actin cytoskeleton, modulates autophagy and inflammasome function.

198 Here we find that the expression of specific inflammasome gene modules stratifies older individuals i

199 85 years of age, the elevated expression of inflammasome gene modules was associated with all-cause

200 ent of additional mechanisms associated with inflammasome gene regulation.

201 the role of DNA demethylation in activating inflammasome genes during macrophage differentiation and

202 ated with ANDRO showed reduced expression of inflammasome genes.

203 NLR family pyrin domain containing 3 (NLRP3) inflammasome has been implicated in HIV-induced microgli

204 NLR family pyrin domain-containing 3 (NLRP3) inflammasome has been shown to play a pivotal role in in

205 y member containing a pyrin domain 3 (NLRP3) inflammasome in a protracted manner, leading to an up-re

206 is field demonstrate the crucial role of the inflammasome in a wide range of disease models.

207 mphocytes, CTL) feedback activates the NLRP3 inflammasome in APCs in an antigen-dependent manner to p

208 how that CHIKV infection activates the NLRP3 inflammasome in humans and mice.

209 emonstrates CXCR2-driven activation of NLRP3 inflammasome in macrophages and indicates a potential ho

210 turation of IL-1beta by inhibiting the NLRP3 inflammasome in macrophages.

211 the more recent discovery of the role of the inflammasome in peripheral and central nervous system cy

212 indicates an unappreciated role of the NLRP3 inflammasome in promoting metastasis via the lymphatics

213 first to report the importance of the NLRP3 inflammasome in regulating the inflammatory response and

214 lammatory pathologies, but the role of NLRP3 inflammasome in these processes is not well understood.

215 p8(-/-) mice revealed a functional Caspase-8 inflammasome in vivo.

216 To counter the damaging action of mtROS and inflammasomes in fully differentiated cells in the retin

217 NLR family pyrin domain containing 3 (NLRP3) inflammasomes in microglial cells and in HIV-Tg rats adm

218 investigate the effect of S. typhimurium on inflammasomes in primary human monocytes.

219 tudies remain uncharacterized on the role of inflammasomes in prostate cancer.

220 o be selective activators of NOD2 and NLRP3 (inflammasome) in vitro but not NOD1.

221 amage-sensing and effector components of the inflammasome, including caspase b, NLRC3 ortholog (wu: f

222 e former group, prime and activate the NLRC4 inflammasome, induce the production of IL-1beta, activat

223 Inflammasome inhibition using CRID3 prevented airway hyp

224 utations of telomere-associated proteins and inflammasomes initiate many chronic human diseases: a hy

225 ltiple sclerosis revealed that autophagy and inflammasomes intersect and regulate each other.

226 ions that are mediated by IL-1beta The NLRP3 inflammasome is a caspase-1-activating multiprotein comp

227 The NLRP3 inflammasome is a central regulator of inflammation in m

228 The NLRP3 inflammasome is a protein complex responsible for caspas

229 How the inflammasome is activated in this untreatable disease is

230 The NLRP3 inflammasome is an intracellular innate immune sensor th

231 rmore, we found that activation of the NLRP3 inflammasome is attenuated in Nrf2-deficient bone marrow

232 e of actin dynamics in the activation of the inflammasome is becoming increasingly apparent.

233 ic Syndromes (CAPS) macrophages, where NLRP3 inflammasome is constitutively activated.

234 NLR family pyrin domain containing 3 (NLRP3) inflammasome is involved in many chronic inflammatory di

235 The NALP3 inflammasome is tightly regulated by recently discovered

236 of NLRC3 on the NALP3 inflammasome or other inflammasomes is still unknown.

237 IL-1beta, which is activated by the inflammasome, is known to be central to the pathogenesis

238 The egested microbes trigger the inflammasome, leading to a rapid production of interleuk

239 c immune cells, pericytes activate the NLRP3 inflammasome, leading to IL-1beta and IL-18 secretion.

240 rmation of a multiprotein complex called the inflammasome, leading to secretion of interleukin-1 (IL-

241 se pseudoviruses activate the NLRP3 and AIM2 inflammasomes, leading to caspase-1-mediated tumour regr

242 Activation of the NLRP3 inflammasome leads to IL-1beta secretion.

243 Also, inhibition of inflammasome led to an increased transcriptional activit

244 netic inflammasome deficiency and that NLRP3 inflammasome-linked inflammation could potentially be ta

245 tently induces pro-inflammatory cytokine and inflammasome-linked transcripts.

246 ense against pathogens, but dysregulation of inflammasomes may contribute to the pathogenesis of mult

247 t macrophages exhibited an increase in NLRP3 inflammasome-mediated interleukin-1beta secretion.

248 iodic fever syndromes caused by dysregulated inflammasome-mediated production of the cytokine IL-1bet

249 repeat and pyrin domain containing 3 (NRLP3) inflammasome members (false discovery rate < 0.05).

250 elucidate the regulation and function of the inflammasome, more evidence has emerged that the inflamm

251 The inflammasome NLRP3 is a molecular pathway activated by a

252 rapamycin-C1/70S6K pathway and activated the inflammasome NLRP3, leading to the release of interleuki

253 eral mechanisms, including activation of the inflammasome NLRP3.

254 However, the effect of NLRC3 on the NALP3 inflammasome or other inflammasomes is still unknown.

255 Targeting NLRP3 inflammasome pathway mediators could thus be developed a

256 and mouse models is driven by a noncanonical-inflammasome pathway that activates caspase-4 (caspase-1

257 ing the transcript levels of the proteins of inflammasome pathways, NLRP3, ASC, caspase 1, IL-1 and I

258 merging evidence suggests that activation of inflammasomes plays a central mechanism in pathogenesis

259 flammation, and dramatically increased Nlrp3 inflammasome priming and activation.

260 This inflammasome priming was due to oxLDL IC signaling via m

261 ch mediates synthesis of pro-IL-1beta during inflammasome priming.

262 Activation of the inflammasome promotes caspase-1-mediated secretion of pr

263 The inflammasome proteins nucleotide-binding oligomerization

264 Inflammasomes regulate innate immune responses by facili

265 Large molecular complexes known as inflammasomes regulate the release of IL-1beta from immu

266 These findings describe a unique pathway of inflammasome regulation with the identification of STAMB

267 We observed that inflammasome-related genes are rapidly demethylated in b

268 BMDCs with oxLDL ICs increased expression of inflammasome-related genes Il1a, Il1b, and Nlrp3, and pr

269 We analyzed DNA methylation levels of inflammasome-related genes in patients with cryopyrin-as

270 Inflammasome-related genes were tested for DNA methylati

271 mechanism of innate immune host defense, and inflammasomes represent a central cytosolic pattern reco

272 -STING-NLRP3 pathway constitutes the default inflammasome response during viral and bacterial infecti

273 describe a coordinated epithelium-intrinsic inflammasome response in vivo.

274 coordinated IEC-intrinsic, Caspase-1 and -8 inflammasome response plays a key role in intestinal imm

275 effect, we comparatively analyzed the NLRP3 inflammasome response to nutrient deprivation in wild-ty

276 n is essential for host defense, deregulated inflammasome responses and excessive release of inflamma

277 0001), consistent with HIV activation of the inflammasome resulting in CD4 T cell depletion.

278 Activation of the NLRP3 inflammasome results in caspase-1-dependent secretion of

279 embled 1.4-megadalton flagellin-NAIP5-NLRC4 inflammasome, revealing how a ligand activates an NLR.

280 The NLRP3 inflammasome senses a variety of signals referred to as

281 ndings are the first to identify NLRP3 as an inflammasome sensor for T. gondii in primary human perip

282 e of TNF-alpha, and indicated a role for the inflammasome sensor NLRP3 and for potassium efflux in T.

283 sets, we screened the expression profiles of inflammasome sensors NLRP3, NLRC4, NLRP6, NRLP12, and AI

284 centre, enabling the formation of one large inflammasome speck complex within a single cell.

285 nflammatory responses through effects on the inflammasome, Th17 signaling and recruitment of phagocyt

286 ed by a cytosolic protein complex called the inflammasome that senses microbial pathogens and then ac

287 16, bind dsDNA and form caspase-1-activating inflammasomes that are important in immunity to cytosoli

288 d with a priming signal, cGAMP activates the inflammasome through an AIM2, NLRP3, ASC, and caspase-1

289 genes identified multiple pathways including inflammasome to be targeted by ZIKV, which was confirmed

290 ly, CARD domain-containing protein 4 (NLRC4) inflammasome upon sensing components of the type III sec

291 d as precursor proteins and activated by the inflammasome via proteolytic processing.

292 QUC inhibition of the inflammasome was still observed in Atg16l1 knockout macr

293 s associated with canonical and noncanonical inflammasomes was detected in patients with TBM-IRIS tha

294 The selected expression of NLRP3 and NLRP12 inflammasomes was validated, and the clinical associatio

295 MPs confer tissue-specific activation of the inflammasomes, we tested the hypothesis that bone matrix

296 e receptor family, pyrin domain containing 3 inflammasome when compared with wild-type mice.

297 The inflammasome, which leads to caspase-1 activation, is im

298 t of the Nod-like receptor protein 3 (NLRP3) inflammasome with canakinumab might alter cancer inciden

299 Upon activation, NLRP3 forms an inflammasome with the adapter ASC, resulting in caspase-

300 mans is dependent on activation of the NLRP3 inflammasome with the subsequent release of IL-1beta fro