ライフサイエンスコーパス: monocyte

1 senting an important reservoir of marginated monocytes.

2 d STAT1 and STAT3 in patient lymphocytes and monocytes.

3 nes involved in TLR signaling in resting UCB monocytes.

4 enes between sarcoidosis and healthy control monocytes.

5 1 and IL-22 induced the expression of H4R in monocytes.

6 e arterial wall and a migratory phenotype of monocytes.

7 xia-inducible factor (HIF)-1alpha in primary monocytes.

8 and to stimulate downstream ERK signaling in monocytes.

9 , IL-6, IL-10, and IL-12 production in human monocytes.

10 ual to pDC from blood and greater than blood monocytes.

11 a in HD11 cells and CCL4 and CCL5 in primary monocytes.

12 g the phlogistic activity of newly recruited monocytes.

13 it ATP-induced mature IL-1beta production in monocytes.

14 ons between irradiated endothelial cells and monocytes.

15 d II interferon stimulation in primary human monocytes.

16 It resulted in the accumulation of Ly6C(hi) monocytes.

17 enables them to stimulate the recruitment of monocytes.

18 1/ATP/P2X7 axis in IL-1beta release by human monocytes.

19 ia-induced gene expression or RNA editing in monocytes.

20 165 trauma, p < 0.0005) and CD14+HLA-DRlow/- monocytes (34.96 x 106/l +/- 4.48 control versus 95.72 x

21 Systemic inflammation through persistent monocyte activation and microbial translocation appear t

22 onocyte-to-macrophage differentiation and on monocyte activation.

23 The concomitant elevation of monocyte activity may provide novel therapeutic targets

24 Monocytes also decreased the expression of M-CSFR, and l

25 knockdown influences NALP3 activity in human monocyte and HEK293FT cells when the complex is ectopica

26 erall, the blood of donors exhibited similar monocyte and lymphocyte content and low serum levels of

27 d the accumulation of cells derived from the monocyte and macrophage lineages, which results in tissu

28 arget protein for treating diseases in which monocyte and neutrophil accumulation is correlated with

29 reduced cytokine release by IFC tissue, less monocyte and T cell migration was detected in a chemotax

30 nt inference revealed a decrease in invading monocytes and a subtype-dependent increase in macrophage

31 nclusion, GPBAR1 is expressed in circulating monocytes and colonic macrophages, and its activation pr

32 reveals enrichment of homeostatic modules in monocytes and DCs from human metastatic melanoma.

33 cterized by increased numbers of circulating monocytes and dendritic cells that produce more inflamma

34 oduce proinflammatory cytokines, and recruit monocytes and dendritic cells to the site of damage thro

35 mmation is largely due to the recruitment of monocytes and dendritic cells.

36 and IL-22 stimulated RANKL expression in RA monocytes and JNJ7777120 reduced the RANKL expression.

37 which HRVs modulate the immune responses of monocytes and lymphocytes are not yet well described.

38 toneal recruitment and adhesive functions of monocytes and macrophages (Mvarphi) and the ability of t

39 Whether monocytes and macrophages are equipped with an allorecog

40 These results support a role for monocytes and macrophages in the pathogenesis of SIV/HIV

41 Bmal1 deficiency in monocytes and macrophages resulted in an increased total

42 yed AD onset and lower expression of SPI1 in monocytes and macrophages.

43 panied by impaired recruitment of Ly6C(high) monocytes and monocyte-derived dendritic cells (moDC) an

44 t stem cells with their cardiac derivatives, monocytes and monocyte-derived macrophages in convention

45 Monocytes and monocyte-derived macrophages promote ather

46 ression of toll-like receptor 2 and CD11b on monocytes and neutrophils, respectively, were observed.

47 Depletion of CCR2(+) inflammatory monocytes and pharmacologic blockade of IL-1beta or NLRP

48 Circulating platelets, aggregates of monocytes and platelets, and activation of microglial ce

49 ogeneous population of human CD14(+) CD16(-) monocytes and prompt further ontogenetic and functional

50 cation and lung infiltration of inflammatory monocytes and T cells in RSV-challenged mice.

51 hesis that depletion of CCR2(+) inflammatory monocytes and their derivatives would abrogate anti-myel

52 We identified both inflammatory monocytes and tissue-resident macrophages as sources of

53 transcripts, and we focus on one cell type (monocytes) and on a small set of highly edited transcrip

54 with glial activation and increased T-cell, monocyte, and neutrophil trafficking to the brain at day

55 Dendritic cells, monocytes, and B cells in HCC tumors expressed ligands f

56 (APCs) in the skin include dendritic cells, monocytes, and macrophages.

57 ng immune cells comprised of CD11b(+) cells, monocytes, and mast cells.

58 and quick binding of HRV types 16 and 1B to monocytes, and slower interaction of these HRVs with CD4

59 Monocytes are a diverse population of cells (classical,

60 onfirmed that approximately equal numbers of monocytes are also recruited in response to this lectin.

61 onocyte subsets indicates that non-classical monocytes are biased progenitors of alternatively activa

62 Two subsets of blood monocytes are commonly described in mice and humans: the

63 Old reports suggest that blood monocytes are distributed into circulating and marginati

64 Blood CD14(+) monocytes are frontline immunomodulators categorized int

65 Monocytes are key players in the development and exacerb

66 Thus LPS stimulated monocytes are partially permissive lytic gene expression

67 e showed that both inflammatory and resident monocytes are retained in the bone marrow vasculature, r

68 In lipopolysaccharide-stimulated human THP1 monocytes, ARID5B knockdown reduced expression of genes

69 l cells and reduced NF-kappaB activation and monocyte arrest on activated endothelium in vitro.

70 antly, it further confirms the role of CD14+ monocytes as an important cellular target for ZIKV infec

71 We identify CD68(+) cells (macrophages/monocytes) as the cryptic EBOV reservoir cells in the vi

72 smablasts, and inflammatory Ly6C(hi) CCR2(+) monocytes, as well as increased levels of proinflammator

73 th BP, such as CXCL10, favor neutrophil- and monocyte-associated MMP-9 release and disease relapse an

74 ng with loss of circulating dendritic cells, monocytes, B cells, and natural killer (NK) cells.

75 the serine/threonine protein kinase TAK1 in monocytes blocked TLR-induced cytokine production and IR

76 Both classical and nonclassical monocytes, but not CD1c(+) DCs, made foamy macrophages e

77 Depletion of inflammatory monocytes, but not DCs or other myeloid cells, resulted

78 Adult bone marrow monocytes can give rise to tissue-resident macrophages d

79 Monocytes can mobilize from bone marrow, traffic to thei

80 ted at various stages, from hematopoiesis to monocyte changes and macrophage activation.

81 tion dynamics of neutrophil, lymphocyte, and monocyte characteristics.

82 Monocyte chemoactive protein 1 (MCP1) has been shown to

83 eficient astrocytes have decreased levels of monocyte chemoactive protein 1 (MCP1) secretion compared

84 rogenase, and inflammatory mediators such as monocyte chemoattractant protein 1 (MCP-1), TNF-alpha, a

85 gration via increased expression of IL-6 and monocyte chemoattractant protein 1 (MCP-1).

86 so increased levels of inflammatory cytokine monocyte chemoattractant protein-1 (MCP-1) and MCP-1 ind

87 We have previously shown that the chemokine, monocyte chemoattractant protein-1 (MCP-1), is a mediato

88 tate dehydrogenase, as well as expression of monocyte chemoattractant protein-1, IL-6, IL-1beta, and

89 micked by stimulation of Hmox1(+/+) SCs with monocyte chemoattractant protein-1, IL-6, IL-1beta, and

90 sis included higher levels of interleukin-8, monocyte chemoattractant protein-1, resistin, soluble in

91 nes for interleukin (IL)-1beta, IL-6, IL-10, monocyte chemoattractant protein-1, tumor necrosis facto

92 necrosis factor-beta, interferon-gamma, and monocyte chemoattractant protein-1.

93 leukin-8/C-X-C motif chemokine ligand 8, and monocyte chemoattractant protein-1/chemokine ligand 2 in

94 ltiple inflammatory mediators, including the monocyte chemoattractant, chemokine (C-C motif) ligand (

95 , vascular endothelial growth factor (VEGF), monocyte chemoattractive protein 1 (MCP-1), and granuloc

96 e sought to identify the RhoGEFs involved in monocyte chemotactic protein 1 (MCP1)-induced vascular w

97 uantified by HPLC/MS/MS, and adiponectin and monocyte chemotactic protein-1 (MCP-1) levels in culture

98 ase reverses endothelial cell activation and monocyte chemotaxis.

99 ic cell clade was distinct from a macrophage/monocyte clade, as supported by higher mRNA expression l

100 Correlations between granulocyte and monocyte clonalities were greatest, followed by correlat

101 RATIONALE: Nonclassical mouse monocyte (CX3CR1(high), Ly-6C(low)) patrolling along the

102 ve in vitro and in vivo assays, we show that monocytes deficient for TNF or TNF receptors are outcomp

103 M. tuberculosis infection, TOLLIP-deficient monocytes demonstrated increased IL-6, increased nitrite

104 Granulocyte-monocyte progenitors (GMPs) and monocyte-dendritic cell progenitors (MDPs) produce monoc

105 However, monocyte depletion significantly reduced glomerular necr

106 treatment and was completely abolished with monocyte depletion.

107 We show that specific genetic deletion of monocyte-derived alveolar macrophages after their recrui

108 During the fibrotic phase, monocyte-derived alveolar macrophages differ significant

109 gues of profibrotic genes expressed by mouse monocyte-derived alveolar macrophages during fibrosis we

110 AE) impairs the accumulation of inflammatory monocyte-derived cells (MCs) in the CNS, leading to impr

111 show that inhibition of HIV-1 replication in monocyte-derived DCs (MDDCs) is associated with an incre

112 96-well in vitro assays using neonatal human monocyte-derived DCs and humanized TLR8 mouse bone marro

113 sults demonstrated that tumour-induced human monocyte-derived DCs exhibited systematic functional def

114 , leaving the immune system and specifically monocyte-derived dendritic cells (MDDCs) understudied.

115 t of Vpr for facilitating HIV-1 infection of monocyte-derived dendritic cells (MDDCs), one of the fir

116 ired recruitment of Ly6C(high) monocytes and monocyte-derived dendritic cells (moDC) and lower moDC c

117 and LAMP-2 (CD107b) on the surface of human monocyte-derived dendritic cells (MoDC) and show only LA

118 -ICs in human B cells and in CD23-expressing monocyte-derived dendritic cells (moDCs) that represent

119 In vitro cultures of different cell types (monocyte-derived dendritic cells [moDCs], PBMCs [periphe

120 GN is a major receptor for infection of both monocyte-derived dendritic cells and interstitial dermal

121 pregulation of CD40, CD80, CD83, and CD86 on monocyte-derived dendritic cells from allergic patients

122 Both fusion proteins matured monocyte-derived dendritic cells through TLR5.

123 oma, infects three types of dendritic cells: monocyte-derived dendritic cells, Langerhans cells, and

124 e rise to a subset of monocytes that yielded monocyte-derived dendritic cells.

125 se to IRI were predominantly newly recruited monocyte-derived inflammatory DCs.

126 erferon gamma by MAIT cells was dependent on monocyte-derived interleukin 18, and was reduced in pati

127 lia is differentially regulated from that in monocyte-derived macrophages and the ramified microglia

128 ith their cardiac derivatives, monocytes and monocyte-derived macrophages in conventional cell cultur

129 Monocytes and monocyte-derived macrophages promote atherosclerosis thr

130 Expression of DHRS9 within a panel of monocyte-derived macrophages was investigated by quantit

131 d enteroid monolayers co-cultured with human monocyte-derived macrophages were used to evaluate barri

132 Monocyte-derived macrophages, located in atherosclerotic

133 tion, local arterial inflammation, driven by monocyte-derived macrophages, predicts future cardiovasc

134 roinflammatory cytokines from mice and human monocyte-derived macrophages.

135 al cells to produce chemokines that localize monocyte-derived mononuclear phagocytes (MNPs) to the me

136 Whereas monocyte-derived TAMs played more potent roles in antige

137 We observe both embryo-derived and monocyte-derived tissue-resident macrophages in a G1-lik

138 In this study, we prepared monocyte-derived tolDCs modulated by dexamethasone and v

139 distinguished Mregs from a variety of human monocyte-derived tolerogenic antigen-presenting cells in

140 BK virus peptide libraries loaded or not on monocytes-derived dendritic cells.

141 ytes toward macrophage differentiation, sJIA monocytes differentiated in vitro toward macrophages, aw

142 We identified TLR7/8 as mediators of monocyte differentiation and M2 MPhi polarization during

143 TLR8 stimulation, independent of HCV, caused monocyte differentiation and M2 MPhi polarization.

144 at IRF4 and MAFB were critical regulators of monocyte differentiation into mo-DCs and mo-Macs, respec

145 we demonstrated that HCV infection leads to monocyte differentiation into polarized MPhis that media

146 te-dendritic cell progenitors (MDPs) produce monocytes during homeostasis and in response to increase

147 rium labeling, we demonstrate that classical monocytes emerge first from marrow, after a postmitotic

148 Inhibition of monocyte exosome release reverses endothelial cell activ

149 completely attenuated collagen expression in monocytes exposed to HCV, and knockdown of TLR7 partiall

150 selectively enhanced CCL2 expression, while monocytes expressed the pro-inflammatory cytokine interl

151 D8(+) T cells for age and CD4(+) T cells and monocytes for sex, we detected a direct effect of these

152 ated critical cell-autonomous role of TNF on monocytes for their survival, maintenance, and function.

153 tly reported that umbilical cord blood (UCB) monocytes from babies born to obese mothers generate a r

154 s achieved by the early release of classical monocytes from bone marrow.

155 Additionally, monocytes from healthy controls, cultured in the presenc

156 Monocytes from healthy volunteers were first primed with

157 Finally, monocytes from patients with type 2 diabetes had increas

158 ment, inflammasome activation is enhanced in monocytes from WAS patients and in WAS-knockout mouse de

159 Here, we dissected the monocyte gene expression profile in childhood obesity us

160 iation of the top 5 differentially regulated monocyte genes in childhood obesity with obesity and com

161 Intermediate and nonclassical monocytes have longer circulating lifespans ( approximat

162 Znrf4 knockdown monocytes have sustained nuclear factor kappa-light-chai

163 ression but did not have long term impact on monocyte identity regarding their differentiation and su

164 begins with a phase mediated by inflammatory monocytes (IM) and proinflammatory macrophages (M1), fol

165 Inflammatory monocyte (iMO) recruitment to the brain is a hallmark of

166 tion of CD4(+) and CD8(+) T cells as well as monocytes in an in vitro human blood-brain barrier (BBB)

167 CAEBV and that implies an important role of monocytes in CAEBV.

168 M2-skewed immunosuppression of non-classical monocytes in conjunction with a global suppression of ty

169 e relevance of the innate immune system, and monocytes in particular, has emerged as an important fac

170 ed through type I IFN signaling and requires monocytes in PBMCs.

171 mCD48 expression on B, T, and NK cells and monocytes in severe asthma was significantly increased.

172 ata suggest a critical role for nonclassical monocytes in the pathology of TBI in mice, including imp

173 eted serum significantly reduced adhesion of monocytes in the presence of human complement.

174 DCs accumulated in the heart coincident with monocyte infiltration and loss of resident reparative em

175 to the RPE layer, followed by (2) subsequent monocyte infiltration from the retinal vasculature into

176 Notably, limiting monocyte infiltration via genetic Ccl2 reduction prolong

177 tor, and chemokines mediating neutrophil and monocyte infiltration.

178 s reported to control the evolution of human monocytes into a refractory state: IL-1R-associated kina

179 d enhanced green fluorescent protein-labeled monocytes into Dysf-deficient BLA/J mice with age-relate

180 ivalis, is shown to drive-differentiation of monocytes into dysfunctional mDCs.

181 ion of LPA that transfigures CD11b(+) murine monocytes into F4/80(+) macrophages.

182 interleukin-4-polarization of human primary monocytes into macrophages results in lower expression a

183 optosis and decreased ingress of circulating monocytes into the joint are responsible for the initial

184 e, resulting in recruitment of CX3CR1+Ly6Clo monocytes into the tumor.

185 nt labeling of intermediate and nonclassical monocytes is consistent with a model of sequential trans

186 1beta and mature IL-1beta release from human monocytes is stimulated by the TLR2 agonists Pam3CSK4 or

187 igher expression of TSLPR and CD127 mRNAs in monocytes isolated from patients with Gram-negative seps

188 ore the possibility that resident macrophage/monocyte-like cells in the cochlea can mediate local aut

189 tion, to quantify the yield of granulocytes, monocytes, lymphocytes and three subsets of DCs from sin

190 ecrosis and crescent formation and abrogated monocyte, macrophage, and dendritic cell increase in the

191 virus with a marked tropism for cells of the monocyte-macrophage lineage, affecting swine species and

192 o inflammatory responses in RAW 264.7 murine monocyte/macrophage cells challenged with the TLR4 agoni

193 n immunodeficiency virus-1 (HIV) targets the monocyte/macrophage lineage at varying stages of infecti

194 s the inflammatory/Th1 responses through the monocyte/macrophage subsets and elicits marked differenc

195 /inflammatory responses elicited by cells of monocyte/macrophage/DC lineages.IMPORTANCE We previously

196 ed by increased accumulation of inflammatory monocyte macrophages and neutrophils in the lungs of mal

197 of male mice, and depletion of inflammatory monocyte macrophages partially protected these mice from

198 ophages in general and Ly6c(hi) infiltrating monocyte-macrophages in particular, accompanied by skewe

199 Monocyte/macrophages of patients with mild cognitive imp

200 LT-1) on neutrophils and to ERV-1/ChemR23 on monocyte/macrophages.

201 ng to hypercellularity within the CNS, where monocytes/macrophages contribute to CNS viremia, neuroin

202 determine if earlier or higher infection of monocytes/macrophages contributes to the more rapid prog

203 imeric) had reduced accumulation of elicited monocytes/macrophages in the peritoneal cavity in respon

204 present a new foundational role for CXCR3(+) monocytes/macrophages in the process of tumor engraftmen

205 ndary bile acids that is highly expressed in monocytes/macrophages.

206 atherosclerosis, due to its active uptake by monocytes/macrophages.

207 hickness ear wounds we found that Arpc2(-/-) monocytes maintain cell speeds and directionality simila

208 A/B and its significant correlation with the monocyte marker CD14 was observed in CAEBV and that impl

209 asing neutrophil extracellular traps whereas monocytes may express TF.

210 sing an in vivo system to observe endogenous monocytes migrating toward full-thickness ear wounds we

211 ents potently synergized with CCL3 to induce monocyte migration and with CXCL8 to stimulate neutrophi

212 mokine was unable to induce transendothelial monocyte migration in vitro and failed to promote leukoc

213 ith a previously unknown function, regulates monocyte migration in vitro.

214 lizing antibodies blocked 15(S)-HETE-induced monocyte migration.

215 Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6C(low) and Ly6

216 ed for efficient early HCMV-induced enhanced monocyte motility and later for HCMV-induced monocyte-to

217 The effect on monocyte number in living mice was assessed after tail v

218 ng an Illumina microarray platform on sorted monocytes of 35 obese children and 16 lean controls.

219 Upon ex vivo stimulation, monocytes of sepsis patients were less capable in phosph

220 work was to study the influence of activated monocytes on clot contraction.

221 However, MPs from leukocytes and monocytes origin were increased in CF patients.

222 pair; however, the contribution of precursor monocyte phagocytic receptors, which are the first to in

223 ons eliminated off-target antibody-dependent monocyte phagocytosis of cynomolgus monkey platelets, an

224 However, monocyte phagocytosis was normal and oxidative burst was

225 Peripheral blood monocytes play a role in sarcoidosis inflammation.

226 ficantly decreased, while the CD14(+)CD16(+) monocyte population was significantly expanded during ZI

227 idase (MPO) is synthesized by neutrophil and monocyte precursor cells and contributes to host defense

228 kewed toward those derived from inflammatory monocyte precursors.

229 Moreover, differentiated monocytes presented with profound transcriptomic, phenot

230 ich uric acid selectively lowers human blood monocyte production of the natural inhibitor IL-1 recept

231 Granulocyte-monocyte progenitors (GMPs) and monocyte-dendritic cell

232 tumor necrosis factor alpha) in circulating monocytes, pulmonary arterial endothelial cells, and als

233 Monocyte recruitment by human HLA antibodies was enhance

234 Furthermore, LDN193189 inhibited monocyte recruitment induced by TNFalpha and BMP9/10.

235 monocytes, suggesting a role for sPrP(c) in monocyte recruitment into the brain.

236 letion promotes atherosclerosis by enhancing monocyte recruitment to atherosclerotic lesions.

237 EC) upregulates VCAM-1 receptors that target monocyte recruitment to atherosusceptible regions.

238 molecules, ultimately resulting in increased monocyte recruitment to the vascular endothelium.

239 at whereas BMP9/BMP10 alone had no effect on monocyte recruitment, at higher concentrations both cyto

240 ecrease of Ccl5 and Ccl8, and a reduction of monocyte recruitment.

241 ATM proliferation, without the bias of early monocyte recruitment.

242 xplore the regenerative effect of reparative monocyte recruitment.

243 d ii) lipopolysaccharide (LPS)-induced human monocyte release of tumor necrosis factor-alpha (TNFalph

244 ith this, we found that LPS-stimulated human monocytes released relatively low levels of ATP, whereas

245 on (IFN)-stimulated genes (ISGs) in infected monocytes remained unclear.

246 factor beta alone, whereas CD14(+) classical monocytes required additional notch ligation.

247 Peripheral monocyte response to lipopolysaccharide stimulation was

248 s advanced PVR is characterized by a chronic monocyte response.

249 Here, the authors examine CD14+ blood monocyte's transcriptome and epigenome signatures to fin

250 Monocytes secrete matrix metalloproteinases (MMPs), whic

251 pes, neither naive nor inflammatory Ly6C(hi) monocytes served as a productive intracellular growth ni

252 the Transwell system, both murine and human monocytes sorted with magnetic beads in the inner chambe

253 Moreover, monocyte-specific p38alpha ablation resulted in a decrea

254 generate transcriptome data from human blood monocytes stimulated with various immune stimuli and pro

255 manner, and the nonclassical blood resident monocyte subset that patrols the intraluminal side of th

256 ly purified human classical and nonclassical monocyte subsets from a clinical cohort, allowing us to

257 Selective labeling of blood monocyte subsets indicates that non-classical monocytes

258 This study suggests that recruited human monocyte subsets trigger a regulatory pathway of cytokin

259 findings, along with our previous work with monocytes, suggest that EGFR likely serves as an importa

260 is of both uninfected and HIV-infected human monocytes, suggesting a role for sPrP(c) in monocyte rec

261 activated yet dysfunctional immune cells as monocytes, T cells, and B cells expressed higher levels

262 al in ischemic tissue is required to attract monocytes that contribute to the angiogenic response.

263 with pancreatic infiltration of inflammatory monocytes that triggered immunopathology.

264 cytes, whereas MDPs gave rise to a subset of monocytes that yielded monocyte-derived dendritic cells.

265 of the FcepsilonRIIb isoform on B cells and monocytes, the expression of the FcepsilonRIIa isoform w

266 (-/-) mice had normal levels of inflammatory monocytes, their NK cells were unresponsive to HSV-2 cha

267 ich is likely linked with the failure of the monocytes to differentiate to a DC phenotype.

268 downregulated during the differentiation of monocytes to macrophages and was not induced in macropha

269 Exposure of monocytes to oxidized low-density lipoprotein, 7-ketocho

270 g bradykinin from HK, Kal directly activated monocytes to produce proinflammatory cytokines, up-regul

271 controls the cyclic trafficking of Ly6c(hi) monocytes to sites of acute inflammation.

272 -) mice also recruited fewer neutrophils and monocytes to the colon during peak infection, which corr

273 led to directly chemoattract neutrophils and monocytes, to induce chemokines and to stimulate downstr

274 monocyte motility and later for HCMV-induced monocyte-to-macrophage differentiation and for the regul

275 lated genes are rapidly demethylated in both monocyte-to-macrophage differentiation and on monocyte a

276 F) significantly activated AMPK and promoted monocyte-to-macrophage differentiation.

277 to identify the viral factor(s) that mediate monocyte-to-MPhi differentiation.

278 which in turn recruited circulating CCR2(+) monocytes toward infection.

279 demonstration that AHR down-regulation skews monocytes toward macrophage differentiation, sJIA monocy

280 Loss of KLF4 in monocytes transcriptionally derepresses Runt-related tra

281 Here we present the CD14+ blood monocyte transcriptome and epigenome signatures associat

282 revealed that CX3CR1 is critical for Ly6Clo monocyte transmigration across the endothelium in murine

283 CD14(+) monocytes treated either with recombinant human IFN-gamm

284 rted previously that a high peripheral blood monocyte turnover rate was predictive for the onset of d

285 caques exhibited higher physiologic baseline monocyte turnover than adults.

286 Circulating monocytes uniformly express high levels of the canonical

287 nia was observed; restoration of circulating monocytes was achieved by the early release of classical

288 ddition of LPS directly to latently infected monocytes was not sufficient to trigger viral reactivati

289 The frequency of CD14(+) monocytes was significantly decreased, while the CD14(+)

290 econstitution with circulating CXCR3-replete monocytes was sufficient to restore engraftment.

291 The effects of monocytes were evaluated using a quantitative optical tr

292 After RA SF and peripheral blood (PB) CD14+ monocytes were treated with histamine, IL-17, IL-21 and

293 GMPs produced a subset of "neutrophil-like" monocytes, whereas MDPs gave rise to a subset of monocyt

294 mice and humans: the classical inflammatory monocytes, which are rapidly mobilized upon inflammation

295 Here, we sought to determine whether monocytes, which can cross tissue barriers, assist ZIKV

296 microglial recruitment of IL-1beta-producing monocytes, which stimulated brain endothelial IL-1R1.

297 natural killer cells, and expansion of blood monocytes with less proinflammatory cytokine response to

298 Treatment of primary monocytes with the NLRP3 inhibitor MCC950 or with extrac

299 We determined this by infecting monocytes with two strains of ZIKV: South American (PRVA

300 g is a prominent new feature of nonclassical monocytes with unique molecular and kinetic properties.