ライフサイエンスコーパス: macrophage activation

1 e the collateral destruction associated with macrophage activation.

2 , from hematopoiesis to monocyte changes and macrophage activation.

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

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

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

6 f lipopolysaccharide-mediated neutrophil and macrophage activation.

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

8 1alpha and aerobic glycolysis that amplifies macrophage activation.

9 ncreased proinflammatory gene expression and macrophage activation.

10 s and correlated with markers of alternative macrophage activation.

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

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

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

14 ogramming of mitochondrial metabolism for M1 macrophage activation.

15 inflammatory cytokine secretion and impaired macrophage activation.

16 modulator of both classical and alternative macrophage activation.

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

18 and alters cytokine production and monocyte/macrophage activation.

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

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

21 CXCL10 that are characteristic of classical macrophage activation.

22 cules, and transcription factors involved in macrophage activation.

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

24 EBPbeta or HIF1 attenuated fibroblast-driven macrophage activation.

25 reases markers of glomerular proinflammatory macrophage activation.

26 rophage activation and inhibited alternative macrophage activation.

27 h Th1-type cytokine production and classical macrophage activation.

28 erial lipoic acid synthetase LipA suppresses macrophage activation.

29 nts with chronic viral hepatitis, reflecting macrophage activation.

30 d lung inflammation, and defective classical macrophage activation.

31 lmonary arteries (bovine and human) regulate macrophage activation.

32 a potent stimulator of alternative monocyte/macrophage activation.

33 pg/ml LPS itself does not trigger noticeable macrophage activation.

34 characterized by uncontrolled CD8 T-cell and macrophage activation.

35 d-HCA2 axis is a novel negative regulator of macrophage activation.

36 ) increased hallmarks of classical pulmonary macrophage activation.

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

38 hepatic expression of markers of alternative macrophage activation.

39 esponse and scar formation by suppressing M2 macrophage activation.

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

41 nvolved in aneurysm formation and downstream macrophage activation.

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

43 ges and microglia, suggestive of mixed M1/M2 macrophage activation.

44 d fibrosis than Chop(+/+) mice, with greater macrophage activation.

45 rotein (TSPO) is a feature of microglial and macrophage activation.

46 and more classical, rather than alternative, macrophage activation.

47 cgr3-rs in the WKY strain leads to increased macrophage activation.

48 lial apoptosis, fibrotic susceptibility, and macrophage activation.

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

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

51 tabolic inflammation, and ER stress enhances macrophage activation.

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

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

54 e involved in the physiological cessation of macrophage activation.

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

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

57 marker in diseases associated with excessive macrophage activation.

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

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

60 3 pathways to induce cytokine production and macrophage activation.

61 s CT administration for in vivo and in vitro macrophage activations.

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

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

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

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

66 ins inherent to ligament healing during peak macrophage activation and angiogenesis may elucidate inf

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

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

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

70 ngs demonstrate that JAK inhibitors suppress macrophage activation and attenuate TNF responses and fu

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

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

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

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

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

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

77 in a feed-forward loop leading to increased macrophage activation and enhanced response of vascular

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

79 legumain activity is highly correlated with macrophage activation and furthermore that it is an idea

80 A. phagocytophilum causes macrophage activation and hemophagocytic syndrome featur

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

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

83 demonstrated that both constitutive alveolar macrophage activation and increased susceptibility to bl

84 r data suggest NK cells regulate monocyte or macrophage activation and infiltration into allografts b

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

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

87 he adipokine system, and increased classical macrophage activation and inhibited alternative macropha

88 ) is a transcription factor that facilitates macrophage activation and innate immunity.

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

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

91 hus, CAST plays a central role in regulating macrophage activation and limiting pathology during infl

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

93 n gamma and interleukin 17, which facilitate macrophage activation and neutrophil recruitment, respec

94 0/STAT3 signalling that promotes alternative macrophage activation and pathological neovascularizatio

95 Tumor cells secrete factors that modulate macrophage activation and polarization into M2 type tumo

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

97 ha, and C/EBPbeta signaling are critical for macrophage activation and polarization.

98 n inflammatory processes and as regulator of macrophage activation and polarization.

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

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

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

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

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

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

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

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

107 ity of arginine controls critical aspects of macrophage activation and reveal a factor for susceptibi

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

109 iseases, we hypothesized that EBP50 mediates macrophage activation and the response of vessels to inf

110 and molecular mechanisms that drive vascular macrophage activation and their functional phenotype rem

111 es chronic cold-exposure-induced alternative macrophage activation and thermogenic gene responses.

112 Macrophage activation and vascular inflammation after ac

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

114 neal cavity, and their effects on peritoneal macrophages activation and in systemic inflammation were

115 dentified type I interferon (IFN) signaling, macrophage activation, and antigen presentation as the m

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

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

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

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

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

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

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

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

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

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

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

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

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

129 ometabolic programs underlying regulation of macrophage activation are unclear.

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

131 proposed as a noninvasive approach to track macrophage activation as a critical event in the develop

132 lymphocytes, and a decrease of monocyte and macrophage activation as a result of PP.

133 igm of IL-4/IL-13-STAT6-mediated alternative macrophage activation as the sole driver of vascular rem

134 lar fungal species in the gut and promote M2 macrophage activation at distant sites to influence syst

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

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

137 Rapid changes in cell volume characterize macrophage activation, but the role of water channels in

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

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

140 Macrophage activation by lipopolysaccharide and adenosin

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

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

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

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

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

146 has also been shown to mediate bone-derived macrophage activation by proinflammatory cytokines.

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

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

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

150 Thus, macrophage activation by the corynebacterial cell wall r

151 Additionally, type I IFN compromised macrophage activation by the lymphoid immune response th

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

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

154 0 receptor and CD206 (markers of alternative macrophage activation) by endometrial macrophages as wel

155 scription factors known to drive alternative macrophage activation, CCAAT-enhancer-binding protein be

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

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

158 anscriptional regulators associated with all macrophage activation complemented by regulators related

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

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

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

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

163 ic diseases and describe how manipulation of macrophage activation could help ameliorate fibrosis.

164 Macrophage activation depended on Toll-like receptor 2 (

165 eity should explain why simplified models of macrophage activation do not explain the extent of heter

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

167 regulator by suppressing T cell immunity and macrophage activation during inflammation, but its role

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

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

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

171 e the role of NADPH oxidase-generated ROS in macrophage activation following FcgammaR engagement usin

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

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

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

175 To investigate the role of macrophage activation in aseptic lung injury and identif

176 These observations suggest that macrophage activation in atherosclerotic lesions results

177 Here, we report microglial/macrophage activation in both a Stargardt disease and ag

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

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

180 The lack of consensus on how to define macrophage activation in experiments in vitro and in viv

181 ework for future research into regulation of macrophage activation in health and disease.

182 However, the manner in which miRNAs regulate macrophage activation in response to different environme

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

184 ate immune response in which zymosan-induced macrophage activation in the retina promotes myelin shea

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

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

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

188 ines chosen to reflect the shifting state of macrophage activation in vivo.

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

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

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

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

193 ransgenic model (IKFM), we demonstrated that macrophage activation increased proinflammatory gene exp

194 onally, we demonstrated that CXCL5 modulated macrophage activation, increased expression of the chole

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

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

197 TF5 does not block macrophage activation induced by TLR2, TLR3, TLR9, or re

198 TM4 and TM6 did not block macrophage activation induced by TLR2, TLR9, or retinoic

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

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

201 epithelial recovery, we investigated whether macrophage activation influences AKI outcomes.

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

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

204 Macrophage activation is a central event in immune respo

205 Macrophage activation is a critical step in host respons

206 Macrophage activation is an important feature of primary

207 Macrophage activation is associated with profound transc

208 Macrophage activation is broadly categorized as classica

209 Proinflammatory macrophage activation is coupled to a metabolic switch t

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

211 Description of macrophage activation is currently contentious and confu

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

213 Alternative macrophage activation is induced by the Th2 cytokines in

214 e role of adenosine in governing alternative macrophage activation is unknown.

215 predicts that IL-10 is necessary to modulate macrophage activation levels and to prevent host-induced

216 sed on three metrics - total bacterial load, macrophage activation levels, and apoptosis of resting m

217 Three macrophage activation markers and 19 cytokines/chemokine

218 with increased expression of the alternative macrophage activation markers Ym1 and Fizz1, increased l

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

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

221 lectively, we propose a common framework for macrophage-activation nomenclature.

222 Ralpha expression in breast cancer cells via macrophage activation of kinase cascades in the cancer c

223 In vitamin D-deficient macrophages, activation of ER stress increased adhesion

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

225 On the basis of studies in mouse macrophages, activation of the nucleotide-binding oligom

226 In mouse macrophages, activation of this pathway requires the pro

227 tor and purinergic receptor signaling during macrophage activation on bacterial infection.

228 Influence of macrophage activation on expression of VE-cadherin/p120-

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

230 The aim of this study is to determine the macrophage activation pathways involved in chronic perio

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

232 ogress has been made in the understanding of macrophage activation, polarization, and function, the t

233 ion within TB granulomas, promoted efficient macrophage activation, protected against Mtb infection,

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

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

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

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

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

239 ade reduced Tbet transcription and abolished macrophage activation, restoring homeostasis in IR-stres

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

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

242 The expression of alternative macrophage activation-specific transcriptions factors, i

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

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

245 g dendritic cells, nor the classification of macrophage activation states as classical versus alterna

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

247 ysis of this data set revealed a spectrum of macrophage activation states extending the current M1 ve

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

249 Macrophage activation status is intrinsically linked to

250 n leukocyte subsets, cytokine responses, and macrophage activation status.

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

252 Macrophage activation syndrome (MAS) is a devastating cy

253 Macrophage activation syndrome (MAS) is an acute episode

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

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

256 auses early-onset recurrent fever flares and macrophage activation syndrome (MAS).

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

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

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

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

261 Macrophage activation syndrome is the rheumatic disease-

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

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

264 ted intravascular coagulation as features of macrophage activation syndrome.

265 e into a life-threatening condition known as macrophage activation syndrome.

266 ut so are cytokines that are associated with macrophage activation syndrome/hemophagocytic lymphohist

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

268 elevated plasma markers of inflammation and macrophage activation, that is, neopterin and sCD14, whi

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

270 tumor cells while lowering the threshold for macrophage activation, thereby providing a universal met

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

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

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

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

275 es in disease states and therapies targeting macrophage activation to promote tissue repair are also

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

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

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

279 more severe toxicity may experience abnormal macrophage activation triggered by the release of cytoki

280 e reveals that IKKbeta inhibits M1 classical macrophage activation two days post infection, which has

281 les, enhanced E2 promoted LC hyperplasia and macrophage activation via ERalpha signaling.

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

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

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

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

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

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

288 M2 macrophage activation was impaired when MMP-28 was absen

289 Extensive microglial/macrophage activation was present in a gradient from the

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

291 receptors (ARs) are important regulators of macrophage activation, we examined the role of A2B ARs i

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

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

294 Several details of crystal-induced macrophage activation were recently uncovered, but very

295 T-cell signaling and macrophage activation were the two primary pathways that

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

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

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

299 ta discussed include the biology of monocyte/macrophage activation with HIV and SIV infection, traffi

300 consensus collection of markers to describe macrophage activation-with the goal of unifying experime