ライフサイエンスコーパス: macrophage activation

1 ever, growth hormone (GH) can also stimulate macrophage activation.

2 ase was evaluated as a marker of alternative macrophage activation.

3 39 deficiency was found to be involved in M2 macrophage activation.

4 e the collateral destruction associated with macrophage activation.

5 , from hematopoiesis to monocyte changes and macrophage activation.

6 e involved in the physiological cessation of macrophage activation.

7 with miR-155 and miR-146a both implicated in macrophage activation.

8 her published findings that MMP-28 regulates macrophage activation.

9 f lipopolysaccharide-mediated neutrophil and macrophage activation.

10 , to a great extent, to the heterogeneity in macrophage activation.

11 d by a positive feedback loop that amplifies macrophage activation.

12 cules, and transcription factors involved in macrophage activation.

13 reases markers of glomerular proinflammatory macrophage activation.

14 d transcription factors that are involved in macrophage activation.

15 erial lipoic acid synthetase LipA suppresses macrophage activation.

16 ted knockdown of TRIM59 enhanced LPS-induced macrophage activation.

17 ction and propose a new role for Cp in early macrophage activation.

18 le of the AP-1 transcription factor c-Jun in macrophage activation.

19 natural killer cell activation, and monocyte/macrophage activation.

20 g the role of the tumor microenvironment for macrophage activation.

21 on gamma, to elicit myeloid infiltration and macrophage activation.

22 tabolic inflammation, and ER stress enhances macrophage activation.

23 pe and is suppressed by IFN-gamma to augment macrophage activation.

24 (+) and CD4(+) T cells, and tumor-associated macrophage activation.

25 rest, NF-kappaB, LPS signaling pathways, and macrophage activation.

26 issue-specific amplifiers of type 2-mediated macrophage activation.

27 marker in diseases associated with excessive macrophage activation.

28 the PDH flux is an important node for M(LPS) macrophage activation.

29 ion inhibitors thereby enabling inflammatory macrophage activation.

30 ges, PARP9 and PARP14 have opposing roles in macrophage activation.

31 3 pathways to induce cytokine production and macrophage activation.

32 suggest that PARP9 and PARP14 cross-regulate macrophage activation.

33 amma or IL-4, that PARP9 and PARP14 regulate macrophage activation.

34 1alpha and aerobic glycolysis that amplifies macrophage activation.

35 ncreased proinflammatory gene expression and macrophage activation.

36 s and correlated with markers of alternative macrophage activation.

37 nscription 1 (STAT1)-mediated classical (M1) macrophage activation.

38 associated protein phosphatase 2A (PP2A) in macrophage activation.

39 s known about their influence on DNA-induced macrophage activation.

40 ogramming of mitochondrial metabolism for M1 macrophage activation.

41 inflammatory cytokine secretion and impaired macrophage activation.

42 modulator of both classical and alternative macrophage activation.

43 and alters cytokine production and monocyte/macrophage activation.

44 s a mechanism by which NaCl inhibits full M2 macrophage activation.

45 kinases (SFKs) to initiate phagocytosis and macrophage activation.

46 CXCL10 that are characteristic of classical macrophage activation.

47 Serum markers of inflammation and macrophage activation.

48 ll-accepted but simplified paradigm of M1/M2 macrophage activation.

49 EBPbeta or HIF1 attenuated fibroblast-driven macrophage activation.

50 ts limited exacerbation of inflammation upon macrophage activation.

51 creased levels of inflammatory cytokines and macrophage activation.

52 iver inflammation, and ER stress can enhance macrophage activation.

53 unity through the blockade of protumorigenic macrophage activation.

54 g the host transcriptome leading to enhanced macrophage activation.

55 tion of AQP3-mediated H(2)O(2) transport and macrophage activation.

56 1s promote adipose fibrogenesis and CD11c(+) macrophage activation.

57 hosphorylation during human monocyte-derived macrophage activation.

58 by the lipoic acid synthetase, LipA, blunts macrophage activation.

59 helial health and endothelial cell-dependent macrophage activation.

60 A-activated protein kinase R (PKR)-dependent macrophage activation.

61 tricarboxylic acid cycle during inflammatory macrophage activation.

62 l electron-transport chain were required for macrophage activation.

63 asured by less cytokine release, T-cell, and macrophage activation.

64 ated by a distinct sensory pathway involving macrophage activation.

65 ly lectins (Siglecs) to block neutrophil and macrophage activation.

66 EGF production and assign obesity-associated macrophage activation a homeostatic role to restore cere

67 was accompanied in the CNS by a decrease in macrophage activation, a decrease in a specific proinfla

68 and previous studies found that alternative macrophage activation accelerates fungal clearance durin

69 nzimidazole inhibitor does not prevent mouse macrophage activation after stimulation with 2,6,10,14-t

70 the effect of therapies targeting microglia/macrophages activation after TBI.

71 vation within macrophages is required for M1 macrophage activation and anti-C. neoformans activity vi

72 icipate in the transcriptional regulation of macrophage activation and are considered potent regulato

73 irect-acting antiviral therapy attenuated M2 macrophage activation and associated liver fibrosis.

74 (-/-) and Ldlr(-/-) mice attenuated monocyte/macrophage activation and atherosclerosis in the absence

75 ated neural damage, whereas csCSF-1 inhibits macrophage activation and attenuates neuropathy.

76 suppressing alpha-SYN-induced microglia and macrophage activation and CD4(+) T-cell recruitment into

77 regulated genes were linked to prevention of macrophage activation and cell lysis, we suggest that th

78 cesses, has been described in the context of macrophage activation and cellular senescence.

79 CD200-CD200R interaction has known to reduce macrophage activation and chronic inflammation.

80 l cord, revealing that LPA induces microglia/macrophage activation and demyelination.

81 We observed similar alterations in macrophage activation and disease phenotype in the Citro

82 d isoforms of CSF-1 have opposing effects on macrophage activation and disease progression in a mouse

83 lts identify heparanase as a key mediator of macrophage activation and function in tumorigenesis and

84 A. phagocytophilum causes macrophage activation and hemophagocytic syndrome featur

85 as a downstream molecular switch controlling macrophage activation and identified extracellular signa

86 inal domain (NTD) mediates the inhibition of macrophage activation and immune functions.

87 dentification of targets, which both prevent macrophage activation and infiltration into islets and r

88 action for SREBPs in augmenting TNF-induced macrophage activation and inflammation and open therapeu

89 imulation had a strong cooperative effect on macrophage activation and inflammatory responses in mice

90 ar leukocytes and macrophages, stimulated M1 macrophage activation and interleukin 10 release, and de

91 The cytokine IFN-gamma coordinates macrophage activation and is essential for control of pa

92 However, spCSF-1 mediates macrophage activation and macrophage-related neural dama

93 0/STAT3 signalling that promotes alternative macrophage activation and pathological neovascularizatio

94 on of CSF1-R and SHP2 signaling pathways for macrophage activation and phagocytosis enhancement could

95 orders as well as molecular studies of human macrophage activation and polarization.

96 lack this metabolic sensor and show reduced macrophage activation and production of IL-1beta during

97 nt macrophages, where it limits inflammatory macrophage activation and promotes a repair phenotype.

98 R91/succinate-dependent feed-forward loop of macrophage activation and propose GPR91 antagonists as n

99 e of mcircRasGEF1B in immune response during macrophage activation and protection against microbial i

100 le of the C-type lectin receptor, CLEC5A, in macrophage activation and pulmonary pathogenesis in a mo

101 as an IgE-mediated mechanism of monocyte and macrophage activation and recruitment to tumors.

102 T cell responses corresponded with impaired macrophage activation and reduced leukocyte accumulation

103 on of inflammatory cytokines associated with macrophage activation and regulated the polarization of

104 rane glycoprotein, in regulating TLR2-linked macrophage activation and resultant proinflammatory resp

105 to Toll-like receptor and by neutrophil and macrophage activation and signaling.

106 duced by OVA, affecting Th2 inflammation, M2 macrophage activation and skin barrier function.

107 A), we investigated Th2 immune responses, M2 macrophage activation and skin barrier gene expression u

108 Specifically, macrophage activation and subtype switching, a key event

109 f genes associated with proinflammatory (M1) macrophage activation and was protective for multiple CN

110 rmatitis was characterized by high levels of macrophage activation, and clearance was associated with

111 as increase local BBB permeability, increase macrophage activation, and decrease the local neural den

112 characteristics in macrophages, phenocopying macrophage activation, and exhibited potent adjunctive a

113 ted events such as eosinophilia, alternative macrophage activation, and immunoglobulin class switchin

114 ted venous beading and tortuosity, microglia/macrophage activation, and increased vascular permeabili

115 panin subgroup more intensely induced during macrophage activation, and its overexpression increases

116 ponse, increased fungal burden, deficient M1 macrophage activation, and loss of protection.

117 r cells (MAPCs) have the ability to modulate macrophage activation, and prior exposure to MAPC secret

118 ophage infiltration into the affected organ, macrophage activation, and release of cytokines involved

119 nsight into the sources of oxidative stress, macrophage activation, and the pathogenesis of lung dise

120 MRP1 expression markedly increased upon macrophage activation, and the role of MRP1 in NO-induce

121 ndent on IFN-gamma production and subsequent macrophage activation, and the Th2 response promotes gra

122 , VASP deficiency induced proinflammatory M1 macrophage activation, and the transplantation of bone m

123 correlates with brain viral load, markers of macrophage activation, and type I interferon responses.

124 Increases in inflammatory markers and macrophage activation are associated with acute AH and c

125 However, the molecular mechanisms limiting macrophage activation are not completely understood.

126 The means by which F. tularensis modulates macrophage activation are not fully elucidated.

127 The pathways that regulate macrophage activation are therefore of great interest.

128 ometabolic programs underlying regulation of macrophage activation are unclear.

129 feron (IFN)-gamma activates genes to promote macrophage activation are well studied, but little is kn

130 Fingolimod treatment reduced microglial/macrophage activation at the site of focal inflammatory

131 d key transcription factors that may control macrophage activation, but experimental validation is la

132 Metabolic reprogramming is implicated in macrophage activation, but the underlying mechanisms are

133 eceptor 2 (TLR2) appears to be important for macrophage activation by corynebacteria.

134 Next, we have inhibited macrophage activation by depleting these cells using clo

135 Outcome of sepsis critically depends on macrophage activation by extracellular ATP-release and a

136 e show that D-mannose suppresses LPS-induced macrophage activation by impairing IL-1beta production.

137 y and proresolving properties while reducing macrophage activation by lipopolysaccharides and enhanci

138 under cell culture conditions, only inhibit macrophage activation by nonviable E. coli In total, thi

139 Anti-CD44 Ab treatment significantly reduced macrophage activation by OA SF (p < 0.01).

140 A CD44-specific Ab reduced macrophage activation by OA SF, and CD44 is a potentiall

141 say platform for high-throughput analysis of macrophage activation by pathogenic stimuli, we generate

142 se data show that VSIG4 negatively regulates macrophage activation by reprogramming mitochondrial pyr

143 se data show that tubular cells can instruct macrophage activation by secreting GM-CSF, leading to a

144 d micro RNA-containing exosomes that inhibit macrophage activation by suppressing Toll-like receptor

145 ta indicate that DUSP11 inhibits LPS-induced macrophage activation by targeting TAK1.

146 Thus, macrophage activation by the corynebacterial cell wall r

147 The involvement of NOTCH signaling in macrophage activation by Toll receptors has been clearly

148 a model in which suppression of alternative macrophage activation by type I IFN during M. tuberculos

149 Mathematical modeling of macrophage activation can improve the understanding of t

150 lated pathway activation but with further Fc macrophage activation, cell death and turnover and activ

151 monocyte apoptosis relative to monocyte and macrophage activation changes remains undetermined.

152 orrelation was identified between microglial/macrophage activation (cluster of differentiation 68 imm

153 T3 haplodeficiency in macrophages attenuated macrophage activation, complete STAT3 deficiency increas

154 jection of EC-EVs in vivo repressed monocyte/macrophage activation, confirming our in vitro findings.

155 inally, using proteomic data, we explore how macrophage activation contributes to our understanding o

156 ukin-4 receptor alpha (IL-4Ralpha)-dependent macrophage activation controlled collagen fibril assembl

157 Three macrophage activation core evolution maps were establish

158 he pathogenesis of cystinosis, biomarkers of macrophage activation could have potential for the thera

159 storm (interleukin-6 median, 135 pg/mL) and macrophage activation (D-dimer median, 5284 ng/mL).

160 Macrophage activation depended on Toll-like receptor 2 (

161 ge-derived ODC is a critical regulator of M1 macrophage activation during both Helicobacter pylori an

162 Like the biblical Tower of Babel, macrophage activation encompasses a panoply of descripto

163 ld-stored grafts in terms of nuclear injury, macrophage activation, endothelium activation, tubulus d

164 f soil organic matter significantly enhanced macrophage activation exhibited by the root extracts of

165 During macrophage activation, expression of IL-1R-associated ki

166 ient selenium induces a phenotypic switch in macrophage activation from a classically activated (pro-

167 the repair phase mediates the transition of macrophage activation from a proinflammatory to a repara

168 lobally searched and reviewed literature for macrophage activation from PubMed databases and screened

169 EMCV-induced macrophage activation has been shown to require the pres

170 visit included measuring four biomarkers of macrophage activation: IL-1beta, IL-6, IL-18, and chitot

171 inhibition of mitophagy triggered classical macrophage activation in a mitochondrial ROS-dependent m

172 tic flush from CC1-deficient livers enhanced macrophage activation in bone marrow-derived macrophage

173 nderstood, and the significance of polarized macrophage activation in controlling AdipoR expression a

174 expression was paralleled by proinflammatory macrophage activation in controls and a noninflammatory

175 ospective therapeutic strategies to modulate macrophage activation in patients with COVID-19.

176 to maintain the negative feedback control of macrophage activation in response to bacterial infection

177 s expressed by resting macrophages, inhibits macrophage activation in response to lipopolysaccharide.

178 Macrophage activation in response to LPS is coupled to p

179 mpanied by a shift toward pro-tumorigenic M2 macrophage activation in Slc7a2-deficient mice, as marke

180 ages, its activity is not crucial in shaping macrophage activation in the adipose tissue during obesi

181 Here, we investigate the role of UCP2 in macrophage activation in the context of obesity-induced

182 with ALS may reflect the extent of microglia/macrophage activation in the white matter of the spinal

183 Despite the global impact of macrophage activation in vascular disease, the underlyin

184 the hyperoxia-induced epithelial MVs promote macrophage activation in vitro and facilitate the recrui

185 the direct effects of STING on SMC death and macrophage activation in vitro.

186 ), and sCD14 and sCD163 (markers of monocyte/macrophage activation) in 39 COVID-19-infected patients

187 oriomeningitis virus (LCMV) can also inhibit macrophage activation, in contrast to Pichinde and Tacar

188 of several markers implicated in alternative macrophage activation including arginase-1 (ARG1) and ma

189 ated with alternative anti-inflammatory (M2) macrophage activation, including interleukin 4 (IL-4), I

190 everal proinflammatory genes associated with macrophage activation, including interleukin-1beta (IL-1

191 , the product of ODC, reversed the increased macrophage activation, indicating that ODC and putrescin

192 compounds can be effective in downregulating macrophage activation induced by lipopolysaccharide and

193 In the process of macrophage activation, induced expression of microRNA (m

194 ing a hypomorphic allele of Nbs1, Nbs1(B/B), macrophage activation-induced ROS caused increased level

195 oup (n = 90), indicating persistent monocyte/macrophage activation, inflammation, and microbial trans

196 Chronic administration of the microglial/macrophage activation inhibitor minocycline to the infla

197 hanisms are required for granuloma assembly, macrophage activation, intracellular parasite killing, a

198 -terminal Hydrolase L1 [UCH-L1]), microglial/macrophage activation (Ionized calcium binding adaptor m

199 Macrophage activation is a critical step in host respons

200 Macrophage activation is an important feature of primary

201 Macrophage activation is attenuated in severe granulocyt

202 Proinflammatory macrophage activation is coupled to a metabolic switch t

203 Since the description of macrophage activation is currently contentious and confu

204 al outcome of inflammatory diseases in which macrophage activation is dysregulated.

205 Fine control of macrophage activation is needed to prevent inflammatory

206 ever, the impact of TDM on IFN-gamma-induced macrophage activation is not known.

207 LR4, macrophage depletion, and inhibition of macrophage activation is protective.

208 we asked whether pro-inflammatory microglial/macrophage activation is required for this process.

209 of the LPS response, and how this may affect macrophage activation, is still unclear.

210 Three macrophage activation markers and 19 cytokines/chemokine

211 ith serum inflammatory, oxidative stress and macrophage activation markers.

212 fected individuals, suggesting that monocyte/macrophage activation may play a role in HIV pathogenesi

213 andida albicans-infected resident peritoneal macrophages, activation of group IVA cytosolic phospholi

214 sclosing an unrecognized metabolic hijack of macrophage activation, our study points towards safe D-m

215 While MKP-2 also modulates macrophage activation, our study suggests that MKP-2 is

216 cted to establish Boolean network models for macrophage activation patterns in response to three diff

217 Cytokine signatures of macrophage activation patterns were identified, providin

218 s have been reported for a complete model of macrophage activation patterns.

219 establish Boolean networks to quantify three macrophage activation patterns.

220 more severe inflammation with an enhanced M1 macrophage activation phenotype.

221 larized these cells to adopt either M1 or M2 macrophage activation phenotypes.

222 trogen, and moisture content) that alter the macrophage activation potential of E. purpurea and deter

223 % to 67.4% led to a 4.2-fold increase in the macrophage activation potential of extracts from E. purp

224 While acute exposure to LPS drives macrophage activation, prolonged exposure to LPS trigger

225 echanism in which IL-6-mediated dampening of macrophage activation protects tissues from overshooting

226 of RXR, granulocyte diapedesis/adhesion, Fc macrophage activation, prothrombin activation and hepati

227 wed binding affinity for LPS which prevented macrophage activation, reactive oxygen, and nitrogen spe

228 nflammatory signals, which through paracrine macrophage activation regulates the migratory phenotype

229 s, but mechanisms linking these phenomena to macrophage activation remain incompletely understood.

230 the contribution of post-initiation steps to macrophage activation remains poorly understood.

231 infection, LipA suppresses pro-inflammatory macrophage activation, rendering these cells inefficient

232 The combined effect of restrained M1 and M2 macrophage activation resulted in decreased production o

233 ignificantly increased circulating levels of macrophage activation (sCD163 and sCD206) markers compar

234 role of Rosi in mediating hyper-inflammatory macrophage activation significant for diseases associate

235 necrosis factor alpha [P = .007]), monocyte/macrophage activation (soluble CD163 [P = .005] and chem

236 ecovery from LPS tolerance leads to a hybrid macrophage activation state that is proinflammatory and

237 the pattern of inflammation depending on the macrophage activation state.

238 e highlight how some of these mechanisms and macrophage activation states could be exploited therapeu

239 the mechanisms that regulate these different macrophage activation states have become active areas of

240 Macrophage activation status is intrinsically linked to

241 Although cytokines that trigger macrophage activation (such as IFN-gamma) induce LGC for

242 ntrations associate with disease activity in macrophage activation syndrome (MAS) and poor clinical o

243 Hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) are life-threatenin

244 features of HLH, using modified HLH-2004 and macrophage activation syndrome (MAS) criteria.

245 Macrophage activation syndrome (MAS) is an acute episode

246 The pathogenesis of macrophage activation syndrome (MAS) is not clearly unde

247 hemophagocytic lymphohistiocytosis (HLH) or macrophage activation syndrome (MAS) occur after chimeri

248 ia in TLR7-overexpressing mice, which have a macrophage activation syndrome (MAS)-like disease.

249 hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS).

250 mphohistiocytosis (HLH), and the HLH-sibling macrophage activation syndrome (MAS).

251 mic juvenile idiopathic arthritis (SJIA) and macrophage activation syndrome (MAS).

252 istoric cohorts of Kawasaki disease (KD) and macrophage activation syndrome (MAS).RESULTSTwenty-eight

253 in response to Ifn-gamma during CpG-induced macrophage activation syndrome and is present at high le

254 neonatal disease includes some hallmarks of macrophage activation syndrome but is much more severe t

255 Hence, sepsis patients with macrophage activation syndrome features may benefit from

256 ospective randomized trial using features of macrophage activation syndrome for mortality risk strati

257 ght contribute to the increased incidence of macrophage activation syndrome in these patients.

258 ammatory disorders and is usually designated macrophage activation syndrome in those settings.

259 n be damaging to the host, as is seen in the macrophage activation syndrome induced by severe infecti

260 is trials, anakinra is effective in treating macrophage activation syndrome, a similar entity with fe

261 d (5) hemophagocytic lymphohistiocytosis and macrophage activation syndrome.

262 ted intravascular coagulation as features of macrophage activation syndrome.

263 Il-18bp knockout (KO) mice with CpG-induced macrophage activation syndrome.

264 usion reactions, dose-limiting toxicities or macrophage activation syndrome.

265 with a cytokine signature similar to that of macrophage activation syndrome/hemophagocytic lymphohist

266 ction, or hemophagocytic lymphohistiocytosis-macrophage-activation syndrome.

267 d model for lipopolysaccharide (LPS)-induced macrophage activation that invokes a mechanism we term q

268 FR deficiency also led to a global defect in macrophage activation that was associated with decreased

269 ns, such as Lassa and Junin viruses, inhibit macrophage activation, the molecular mechanism of which

270 Lactate dehydrogenase (LDH) are required for macrophage activation, their bactericidal function, and

271 During proinflammatory macrophage activation, there is an accumulation of the K

272 bolic components of TLR responses to enhance macrophage activation; they also provide insights for IF

273 cause GSTP1 and MRP1 are up-regulated during macrophage activation, this investigation examined wheth

274 factors produced by PELP1-cyto HMECs promote macrophage activation, THP-1 macrophages were treated wi

275 ivation, complete STAT3 deficiency increased macrophage activation through compensatory upregulation

276 functional TLR4 reduces oxidative stress and macrophage activation to decrease TGF-beta-induced extra

277 is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome.

278 of an M2-like phenotype in late stages of M1 macrophage activation to promote wound healing.

279 CD74 downregulation leads to altered macrophage activation toward a proinflammatory signature

280 AT3, STAT5, p38, and ERK1/2), redirection of macrophage activation toward a prorepair phenotype, and

281 ion to the proliferative phase and modulated macrophage activation toward the M2 phenotype that promo

282 ified, providing a possible determination of macrophage activations using extracellular cytokine meas

283 ediators of acute lung injury triggering the macrophage activation via Toll-like receptor 4.

284 on of the innate immune system and microglia/macrophage activation via Toll-like receptor 9 using CpG

285 Surprisingly, diminished M1 macrophage activation was also detectable, as marked by

286 We showed that M2 macrophage activation was associated with liver fibrosis

287 Liver damage was fully abrogated when macrophage activation was blocked using anti-CSF-1R mAb.

288 The shift toward M2 macrophage activation was confirmed in bone marrow-deriv

289 Pro-tumorigenic M2 macrophage activation was diminished in myeloid-specific

290 cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair afte

291 cible nuclear protein Ipr1 as a biomarker of macrophage activation, we performed a high-throughput sc

292 ated lesions with axonal loss and microglial/macrophage activation were also observed.

293 The alterations in M1 and M2 macrophage activation were confirmed in bone marrow-deri

294 malian chitinase (AMC), their size-dependent macrophage activations were modified, at least in part,

295 TRIM59 significantly suppressed LPS-induced macrophage activation, whereas siRNA-mediated knockdown

296 ptive immune system suppresses antibacterial macrophage activation, whereas the innate lymphoid syste

297 tween miR-155 and miR-146a expression during macrophage activation, which creates a combined positive

298 macological inhibition of mitophagy promoted macrophage activation, which favored bactericidal cleara

299 ncreased classical and decreased alternative macrophage activation, which in turn cause insulin resis

300 Dissecting the regulation of macrophage activations will have a significant impact on